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From: ((Steven B. Harris))
Subject: Re: Hydrogenated foods
Date: 24 May 1995

In <> (Brian
Manning Delaney) writes:

>['n' = 'omega']
>In article <3p7duj$>,
> (Steve Harris) wrote, among other things:
>>In <> (Brian
>>Manning O Dubhshlaine) writes:
>>>Heck, why not olive oil? (Not actually too different from
>>>your suggestion [to use non-hydrogenated oil-based margarines].)
>>>For some purposes it might not be
>>>the right taste, but for bread/toast, for ex., it's pretty
>>>good. It's becoming a standard in many restaurants (and has
>>>been for years in most Italian restaurants).
>>  Only cause I hate olive oil; no other reason.  As a food oil and
>>butter substitute it's (biochemically) excellent (gag).  Was it
>>Godfather III where they're all down in the basement drinking olive oil,
>>neat?  <double gag>.
>Fair enough, but from the standpoint of your profession (or
>simply of the advocacy role one adopts in Usenet) might be
>worth mentioning to others ("it might make you want to puke,
>but I care about my patients, so try this..").

Comment: I dunno what your beef here is.  I made my personal bias clear
enough, and gave the science.  You don't get both that often, and now
you're carping that I *still* fumbled it?  Boy, you have got anal
retentive standards.  I'm not working here, remember?  I've a volunteer,
and I didn't volunteer for YOU.

>More importantly, my hunch is that we'll discover some day
>that at least ome people need _particular_ n-3's, not just
>any old n-3. For ex., there is some evidence that the
>elderly can't control conversion from shorter chain n-3's
>(the one in plants -- 18:3 or linolenic) to the longer ones
>(found in fish in abundance -- 20:5, EPA, or 22:6, DHA).

Yeah, and it's not even clear if kids are as good at it (ALA --> DHA,
EPA conversion) as they need to be optimally.  It's primarily the
growing brain that needs a lot of DHA, and I've sometimes wondered if a
bit of fish oil in the first two years of life might not help out with
this task a LOT.  By God, maybe codliver oil does have some of the
magical properties ascribed to it by parents of centuries past, and it's
not the A and D in it at all.

>And it could even be (Slightly Informed Guess Dept.) that
>people who grow up eating a lot of fish lose the ability to
>convert (or to convert readily) the shorter n-3's to the
>longer ones. I'm thinking here of studies of indigenous
>folks in Canada -- could be a genetic thing; I'm not saying
>vegetarianism is inherently dangerous.

   Would be an interesting study.  You need brains of elderly eskimos of
four groups: 1) raised on fish, then switched to prepackaged junk, 2)
Raised on formula, switched later to fish, and then (3 and 4) the two
groups that have eaten the same thing all the way through.  FA analysis
would be fascinating.

>  [And, BTW, we need the longer ones to produce the
>hormone-like things generally known as eicosanoids -- but
>too many might be prob'atic too, thus concern re elderly.]

I don't think it's been proven that the 3-series prostaglandins are
necessary.  They do get produced out of EPA, but that's not saying that
we'd miss them if they weren't.

                                               Steve Harris, M.D.

From: ((Steven B. Harris))
Subject: Re: Flax Seed Oil
Date: 17 Jun 1995

In <3rv7a6$> (Sylvan
Freeman) writes:

>Sorry if this has been addressed before, but can anyone give me
>information about flax seed oil reducing cholesterol?  If this has
>already been discussed, you can email me.

All polyunsaturated oils reduce cholesterol.  Flax is nice because it
also has lots of alpha linolenic acid, an essential fatty acid.  It
oxidizes extremely fast, though, and needs to be bought cold-expressed,
kept in the refrigerator, used up in a couple of weeks (small bottles),
and even had some vitamin E added when you open a new bottle.  It should
also be only used for salads-- I wouldn't use it to fry or even bake.

                                             Steve Harris, M.D.

From: ((Steven B. Harris))
Subject: Re: Foods containing Essential Fatty Acids???
Date: 22 Jun 1995

In <> (Paul Iannone) writes:

>In message ID <3san0f$k7q@nntp.Stanford.EDU> on 6/21/95, Eric Alan Braun
>: Does anyone know which foods contain the essential fatty acids:
>:  Omega 3 & 6
>:  Gammalinolenic Acid
>: Thanks in advance for the info!
>: .eric
>Omega 6, you name it. EVERYTHING. Omega 3, cold temp weeds, mostly. Stuff
>most of us don't eat anymore. Fish from cold water.
>GLA, some wierd herbals like borage and evening primrose.

And blackcurrent oil, which is probably the best buy.  It avoids the
possible poisonous alkaloids of borage, but has a good deal more GLA
than evening primrose.  GLA is omega-6, BTW, dispite being named as a
linoleNic acid.  A sourse of endless confusion to many.

                                              Steve Harris, M.D.

From: ((Steven B. Harris))
Subject: Re: Essential Fatty Acids
Date: 29 Jun 1995

In <3shvns$> (Jason
Taylor) writes:

   >> In regards to the food connection, it is known in
mammals that diet does affect the type of oils in the body;  one
art. in Sci.News I read discussed feeding chickens fish oil to
successfully make them have egg yolks very high in omega-3.  One
uncomfirmed source I know of reports that only fish that eat
plankton have high PUFA levels. <<

    Comment: Yes, dietary fat composition has an immense effect
on body fat composition, since in actuality very little fat is
synthesized de novo from carbohydrate (at least in carnivores and
omnivores).  Pigs, for instance, are fed beef fat all the time to
give the bacon that nice white marbling.  But if you feed pigs
lots of fish or linseed oil, even with adequate vitamin E, you
get a slimy sort of bacon that is (presumably) healthier to eat,
but which will not sell.

   You can easily tell a human's past dietary composition, plant
vs. animal, from a fat biopsy.  Here, you are indeed what you
eat.  Big-time eaters of animal fats may be called "lard butts"
as metaphor, but in fact it's not that far from the truth.

                                      Steve Harris, M.D.

From: ((Steven B. Harris))
Subject: Re: Essential Fatty Acids
Date: 01 Jul 1995

In <> (Steve Chambers) writes:

>In <3sv2ks$> ((Steven B. Harris)) writes:
>>    Comment: Yes, dietary fat composition has an immense effect
>>on body fat composition, since in actuality very little fat is
>>synthesized de novo from carbohydrate (at least in carnivores and
>>   You can easily tell a human's past dietary composition, plant
>>vs. animal, from a fat biopsy.  Here, you are indeed what you
>>eat.  Big-time eaters of animal fats may be called "lard butts"
>>as metaphor, but in fact it's not that far from the truth.
>And fat cells are not the only ones heavily influenced by the balance of
>various fats in the diet. For example, they make their way into cell
>membranes, changing the properties of those membranes, the activity of
>receptors in those membranes, and the balance of various factors which
>are synthesised using lipids from those membranes (eg. leukotrienes).
>IMNSHO dietary fatty acid balance is a grossly under-researched area -
>particularly since the profile of current fat consumption is way
>different from that of most of our evolutionary history.

Particularly if you count the trans stuff <gak>.   I'm with you--
there's a lot of therapeutic power totally untapped here, because we
have no idea what we're doing yet.  Fortunately, all the experimentation
is pretty harmless.  I've been much impressed lately at how much you can
influence inflammation in some people (though not, unfortunatly,
everyone) by cutting their agro meat and dairy, and feeding them fish
and plant oils-- w-3's (EPA, DHA, ALA), and the w-6 GLA.  So much so,
that I now think that dietary fat manipulation (surely fairly safe)
ought to be tried first in anyone who is considering going on chronic
NSAID treatment (dangerous as Hell, statistically).  It appears that
some of these snake oil/ raw veggie cures for people with "rheumatiz"
and various chronic ailments are not quackery.  But I always suspected

                                             Steve Harris, M.D.

From: (Steven B. Harris )
Subject: Re: Lecithin Question
Date: 24 Sep 1995

In <442col$> (Bill Hay) writes:

>Steven B. Harris ( wrote:
>>    It's better not to waste your money!  Lecithin does not lower
>> cholesterol any better than an equal weight of corn oil. And neither
>> one is all that safe to use for the purpose, due the large amounts of
>> polyunsaturated fat you're getting.
>I'm thinking of taking lecithin for two reasons. First, it's a good
>source of choline. Choline has a wide range of beneficial effects (and
>although DMAE might be more effective in many situations for cognitive
>enhancement, choline does a lot of things that DMAE doesn't). And the
>second reason is that I want the polyunsaturates! Soy lecithin (and
>soybean oil) have a good balance of linoleic and linolenic acid, both of
>which are classified as essential fatty acids. I could take GLA or EPA
>which those acids form, but I am sensitive to them when I take them
>My main concern with lecithin is that it can go rancid (and actually
>starts to go rancid before it is noticeable by taste).
>Bill Hay, Norfolk VA (

   Since DMAE is converted directly to choline, I'm skeptical that
choline does things DMAE doesn't.  But who knows?

   Agree about soybean oils' excellent fatty acid composition, but
that's only an argument to eat soy products, not necessarily lecithin,
which (as you point out) has usually been processed and oxidized to
death.  For omega-3's you're better off with a couple of teaspoons of
unrefined flaxoil which has been processed by one of those companies
that takes super care in doing it, and supplies it in refrigerated
brown bottles, under nitrogen.   See you largest health food store.  If
they don't maintain a refrigerator for oils, they don't know what they
are doing.  Find one that does and check out the flax products.

                                        Steve Harris, M.D.

From: (Steven B. Harris)
Subject: Re: Eicosapentaenoic Acid (EPA)
Date: 27 May 1996

In <4occis$> (Carolyn699)

>     I bought some of this.  Now could someone tell me what it is good for?
>The bottle says it is a dietary supplement.  I don't notice anything when
>I take it.
>                     Thanks for your help,     Carolyn

   Geez, will you take anything that is sold in a capsule? :-0

   EPA is pronounced "I koza penta EEEN oh ik acid" (saying it this way
will get you into the organic chemist's club).  It is 20:5w3, a fat
which has fatty acid residues composed of 20 carbons with 5 alternating
double bonds, starting 3 carbons from the CH3 end of the lipid residues
of the molecule.  (Eicosa = 20 in Greek, and the "penta and EN-OIC"
refer to the five double bonds).  EPA is a highly unsaturated component
of many cold water fish fats, and as an oil with a low freezing point,
helps fish stay flexible in very cold water.  It's also a minor
component of human brain (it is a precursor of a more common brain
lipid containing residues of DHA, which is 22:6w3).  EPA can be made
from ALA, but is more easily obtained from the diet, mostly from fish.
Large doses of EPA (5 grams a day) lower serum cholesterol, and have an
anti-platelet and anti-inflammatory effect, due to the synthesis of
certain 3-series prostaglandins from EPA.  This may favorably effect
atherosclerosis and arthritis, although the side effects from
inhibition of clot formation may make EPA ingestion a mixed blessing.
Eskimos have more hemorrhagic strokes than the average Westerner, and
EPA may be the reason.

                                             Steve Harris, M.D.

From: B. Harris)
Subject: Re: Any problems with peanuts/peanut oil?
Date: Sun, 17 Nov 1996

In <> (DIANE
GRAYSON) writes:

>In article <56h43s$>
> B. Harris) writes:
>>   Yes, the order of residues in the triglycerides of peanut oil
>>promotes atherogeneis for some reason.  When the oil is scrambled and
>>resynthesized, mixing up the order of fatty acid residues but keeping
>>the total residues the same, the effect disappears.
>>                                           Steve Harris, M.D.
>That sounds interesting.  What does it mean?
>          Diane

   It means that peanuts and peanut oil promote heart disease and
stroke.  They have proven to do so in monkeys, so this isn't just
theoretical. And if anybody tells you it cannot be so because the fats
in peanut oil are polyunsaturated, this only means they aren't up to
date.  There's more to the goodness or badness of fats than what's in
the side chain of the fatty acid residues.

   If you must have nut butters and nut oils, I highly recommend almond
butter and almond oil.  Hazel nut butter is also excellent on
sandwiches (though a bit stronger in taste).   All these are high in
monounsaturates, like olive oil, and lower cholesterol and cut risk of
heart disease.  These are available in many large supermarkets, and
you've probably passed them every day without noticing.  Take a stroll
past the Jiff isle and let old George Washington Carver spin in his
grave in the goober pea field.

                                              Steve Harris, M.D.

From: B. Harris)
Subject: Re: GLA
Date: 09 May 1997

In <> (Steve Chambers)

>Marty wrote:
>> GLA can increase prostaglandins of the 1-series but it's biggest effect
>> is often on elevating arachidonic acid levels and increasing
>> prostaglandins of the 2-series.
>> Beneficial effects of GLA are highly dose dependent.  Doses of 2 grams
>> or more per day of GLA really push arachidonic acid formation and end
>> up being pro-inflammatory.  Because of this dose effect, evening
>> primrose oil turns out to be safer to use than borage seed oil (because
>> evening primrose oil has a low GLA content).  GLA has already been
>> linked to epilepsy and mania, primarily because most people have no
>> idea how to properly use it.
>Just so I'm clear on what you're saying here - Gamma LinoLENic acid
>drives Arachadonic Acid production?  How does this work?

   Gamma linoLENic acid (GLA, the stuff to get which people take
borage, EPA, and black current oil) is actually omega-6.  While
alpha-linolenic acid or ALA (typically sought in linseed and canola) is
omega-3.  They are both linoLENic acids.  Go figure.  In any case, the
omega-6 fatty acids lead to the 1 and 2 series prostaglandins, and the
omega-3 ALA is converted through DHA and EPA to 3 series

                                       Steve Harris, M.D.

From: B. Harris)
Subject: Re: FAT
Date: 15 May 1997

>In article <5lcmef$odv$>, mm <> wrote:
>>Talking with a cell biologist, I was told that a very low fat diet is
>>actually detrimental because after a length of time, the body ceases to
>>produce the fat processing enzymes. It was also said that fat is
>>necessary to the body's well-being. My contention is that no one
>>actually achieves a fat free diet, only comes close and that the body
>>can do fine on 10 grams of fat or less per day. Anyone know?

   Linoleic and alpha-linolenic acid residues in fats cannot be made by
the body, and are essential, like vitamins.   You'd certainly run into
deficiency on 10 grams of total fat per day.

                                       Steve Harris, M.D.

From: B. Harris)
Subject: Re: Vegetarianism and omega-3 fatty acids
Date: 21 May 1997

In <> Perdita Stevens
<> writes:

>Standard nutrition texts cite oily fish as the main source of omega-3
>fatty acids. I know some vegetable oils also contain them: but as far as
>I know all of those contain a lot of omega-6 fatty acids as well. (In
>particular, more than k grams of omega-6 per gram of omega-3.)
>Unless I'm missing something (e.g. there's some vegetarian source of
>omega-3s that I don't know about) this means that it's impossible for a
>vegetarian (someone who doesn't eat meat or seafood products, but does
>eat dairy produce) to get a recommended ratio of omega-3 to omega-6 fatty
>acids in the diet.
>Is this right? And as a vegetarian, should I be concerned about this?
>Does anyone out there have an opinion (the more supported the better!) on
>any of these matters? In particular, how reliable, if at all, is whatever
>evidence there is that the ratio matters?
>Thanks for any comments,
>Perdita Stevens

    I think the recommended ratio for essential fatty acids in animal
feed is somewhere around 10 to 1 omega-6 (linoleic) to omega-3
(alpha-linolenic).   That, at least, is about the ratio of their daily
requirements (which in humans run something like 5 grams and .5 grams).
 Corn oil does indeed run a high ratio-- something like 30 to 1.   I've
read somewhere that hemp oil (hard to get but not illegal and not
impossible) has a better nutritional ratio.

   In the absense of exotic hemp oil, you will need to blend high
omega-6 oils with high omega-3 oils, which do exist.  Unhydrogenated
Canola is something like 10% omega-3, and much of the rest is
monounsaturated (not an essential omega-6), so the omega-6 to 3 ratio
is very low.  I believe that linseed oil (50% ALA) has more omega 3
than it does omega 6 also.

                                             Steve Harris, M.D.

From: B. Harris)
Subject: Re: "Fats that heal, fats that kill" book
Date: 25 May 1997

In <>
Alex Brands <> writes:

>Mark Thorson wrote:
>> In article <>,
>> Alex Brands  <> wrote:
>> >On Fri, 23 May 1997, Mark Thorson wrote:
>[debate on why flax seed oil does/does not need to be kept cold]
>> Would a house burn down faster on a hot day in summer rather
>> than a cold day in winter?  All other factors (such as humidity)
>> being equal, you wouldn't be able to measure the difference
>> caused by temperature.  It just isn't relevant.
>The example you give is a reaction that is so exothermic that it becomes
>self sustaining, and the surrounding temperature becomes insignificant.
>The actual reaction taking place, the conversion of cellulose to carbon
>dioxide and water, is temperature dependent.  The fire doesn't start
>until some piece of the wood gets hot enough.
>I guess what you're saying is that the rate of the reaction we're talking
>about is so slow in the absence of light, that it's not likely to happen
>at common household temperatures.  A better analogy would then be: is a
>piece of wood more likely to spontaneously catch fire at room temperature
>than in a fridge?  Formally, the answer is yes, but realistically, it's
>not going to happen at either temperature.
>> >Mark, you're posts are very confusing.  It seems that a lot of us
>> >think that the oils fed to the pigs in that study were rancid.  The
>> >only "reason" you give to believe otherwise is because nowhere in the
>> >description of the experiment do they say that the oils were rancid.
>> >This has no resemblance to logic whatsoever.  Did they keep those oils
>> >in seeled, light-tight containers until they fed them to the pigs?
>> >They didn't mention anything like that either.
>> The USDA report mentioned the relevant facts.  Some people
>> are leaping to the conclusion that other conditions were also
>> present because that would be consistent with the quack nutritional
>> theories taught by Erasmus.
>From what I gather, there is no mention at all of these conditions, one
>way or the other, in the description of the study.  If this is so, then
>the study is flawed, and we can't really draw any conclusions from it.
>> Getting back to the silly idea that refrigeration of flaxseed oil
>> is helpful to preserving it, why would Erasmus propose such a
>> notion if it ain't true?  I can't get into his head and give you
>> a certain answer, but I would guess it's to add ritual to the
>> practice of eating flaxseed oil that he promotes.
>If you have a sealed jar of flaxseed oil, then you open it to take some
>of the oil out, will the remaining oil be better preserved at low
>temperatures?  I don't know, but even if it isn't, it doesn't hurt, does
>it?  If you don't have room in your fridge for a bottle of oil, you
>should probably get rid of some of those old bottles of salad dressing.

    Comment: this who discussion is a bit surreal.  Spontaneous
combusion in oily rags soaked in pain thinners, is CAUSED by room
temperature oxidation of linseed oil in them.  This can happen in
garbage cans in hours--- it doesn't have to take place in your attic
over days.  Linseed oil is horribly dangerous if you give it a wick--
the only way to safely get rid of the stuff on cloth, is to put in a
metal paint can half full of water, and throw THAT out.

   The reason linseed oil is a major component of "drying oils" and
"oil based paints" is because the "drying" of such paints is nothing
but oxidation of oils of linolenic acid.  Paint a wall with oil paints
and over the next few days the stuff "burns" into a sort of crosslinked
amber.  If the surface area wasn't so large, and the paint coating so
thin, the heat generated would be hazardous.  As it is, the free
radicals generated cause respiratory problems to people in the room,
deteriorate photographic prints, and generally cause all kinds of
problems we usually associate with smoke.

   Yes, linseed oil oxidizes rapidly in air at room temp.  It's hard to
think of a common hydrocarbon more unstable.

                                          Steve Harris, M.D.

P.S.  Although linseed oxidation is temperature sensitive, it's not as
sensitive as most chemical reactions, since it's a free radical process
with a very low energy of activation.  In general, the reaction is
limited by diffusion factors which limit oxygen availability, so
temperature is not the chief thing slowing up the reaction (oil based
paints "dry" reasonably well even in cold temps).  Keeping the stuff in
a sealed bottle is the main thing.

From: B. Harris)
Subject: Re: help with linolenic acid
Date: Wed, 09 Jul 1997

In <5pv71c$> (richard) writes:

>this maybe a silly set of questions but i was wondering...
>what is linolenic acid?
>would an extra 200 mg a day be bad for a person?
>would it (or oleic acid) add to cholestrol levels if one had 200 mg more a
>thanks in advance.

   Linolenic acid residues in plant oils come in two common varieties:
alpha linolenic acid (an omega-3 residue), and gamma linolenic acid (an
omega-6 residue).  The first is an essential fatty acid.  The second is
a metabolite of another essential fatty acid (linoleic).  Neither of
these raises cholesterols, and (in any case) 200 mg is a not very much
of either.  An average American diet supplies a gram of alpha
linolenic, for instance.

                                            Steve Harris, M.D.

From: B. Harris)
Subject: Re: Canola/Rape, cooking II
Date: Sat, 11 Oct 1997

In <> Paul LeBlanc <> writes:

>The following at least confirms that Canola and Chinese Rapeseed are
>different but quite comparable in their ability to produce Aldehydes,
>etc. when heated.  The numbers indicate that peanut is significantly
>safer to cook with than either soy or Canola.
>At least this clears up the confusion about the differences that might
>exist between Canola and Rapeseed for cooking (virtually none). - paul

   Comment: and not suprisingly, since very likely the source of these
nasty things is the relatively high (10%) content of omega-3
alfa-linolenic acid (ALA) in the Canola, which isn't affected by the
breeding and purification program to rid it of erucic acid residues.
I would expect that hydrogenated Canola would have much superior
properties as a cooking oil, with regard to free-radical and oxidation
products.  But then, the stuff is hydrogenated, and you have 10%
hydrogenated compounds in it, which act much like saturated fats in
their effect on cholesterol.

    Don't cook with high ALA oils like unhydrogenated Canola and
linseed!  ALA oxidation is what makes drying oils "dry," and it's what
makes them spontaneously combustable (ALA oxidation happens so fast
that even at room temp you can get heating to fire point).  ALA needs
to be kept cold and protected from oxygen.  Fail to do this, and you
pay the price.

    And stay away from other polyunsaturates when cooking.  Fry with
olive or almond oil.

                                           Steve Harris, M.D.

From: B. Harris)
Subject: Ghee-- ha!      (was: Frying/ Canola/Rape, cooking II)
Date: Tue, 14 Oct 1997

In <61tsen$> (turf)

>For any high heat frying, the best fat that is inexpensive and
>widely available is ghee.  Make it yourself (from my web page
>recipe section):
>======================== Ghee =======================
>1 or 2 lb unsalted butter
>Salt, if desired - Morton's Lite Salt or Hain's Sea Salt or
>Baleine Sea Salt.
>Put a pound or two of unsalted butter in a saucepan and heat on
>medium/high until it boils.  Skim foam as it forms.  Then, turn
>down the heat to low and stir occasionally.  After about 20
>minutes, the butter will clarify and the solids will sink to
>the bottom of the pan.  After another 5 minutes or so, the
>solids will brown.  It is then done.  Strain through multiple
>layers of cheesecloth into a canning jar.  Refrigeration is not

   Comment:  Something almost commically bad-- a recipe for oxidized
cholesterol in soup of saturated fat.  Yum.

    Ghee is probably the reason why all those vegetarian Hindus really
don't get the benefit out of their lifestyle you'd think they would.

                                  Steve Harris, M.D.

From: B. Harris)
Subject: Re: High Cholestrol
Date: Mon, 01 Dec 1997

In <65rmie$i1r$> (J.
Mark Taylor) writes:
>"A & S" <> wrote:
>>When reading labels. Is it the fat grams or cholesterol grams you look
>>to avoid. Just need a help on this subject.
>Neither. That rather useless dietary label serves only to obfuscate
>good dietary practice. You should instead be reading the ingredient
>You should be reading the ingredient list as a matter of habit so that
>consumer purchasing power can be brought to bear against the
>manufacturers of dubious food-like substances.
>The bad boogie of cholesterol is a myth. My advice to you would be to
>get cholesterol medical dogma out of your head entirely.
>Of primary importance when it comes to foods is good fats vs bad fats.
>Good fats are natural fats & oils. Good fats are butter, tallow, lard,
>olive oil, almond oil, safflower oil, etc..  Bad fats are
>man-contrived, artificial substances. Bad fats are margerine,
>shortening, modified oils and hydrogenated oils of any type or source
>-- they all contain large amounts of trans fatty acids.The ingredient
>list will show these items accordingly.
>Restaurants will almost invariably use hydrogented oils as they are by
>far the cheapest and their use maximizes profit.
>I recommend that consumers use their purchasing power to avoid oils
>derived from genetically engineered crops, too (just on principle).
>These would include all American soy oils and Canadian Canola oil.
>Most plant oils are yellow or red in color. If the liquid oil you are
>buying is clear then it has been very highly processed necessarily
>resulting in increased trans fatty acids. Buy extra virgin olive oil
>when in doubt.
>The decision to avoid trans fats is the single greatest
>health-improvement choice that a consumer may make. I cannot emphasize
>this too greatly.

   What a bunch of malarky.  You'd think nobody ever died of heart
disease before hydrogenation was invented.  I've got news for you: The
Irish and the Finns have being dying at right rates from heart disease
for more than 60 years, and the rural rates (where people persist on
their own butter and cream) have been even higher than the urban rates.
As have the cholesterol levels.

   Both trans fatty acids and saturated fatty acids from dairy products
(particularly palmitic and myristic acid) raise cholesterol levels
efficiently.   There are excellent correlations between blood
cholesterol and heart disease, and quite enough evidence that
cholesterol is a major causative agent in atherosclerosis.  Do whatever
you have to do to get cholesterol down.  That means avoid dairy fat and
hydrogenated fat, in particular, and (to a lesser extent), meat fat.
Margarines are perfectly okay if they are *liquid,* and hydrogenated
fat is minor ingredient in them (say, third or fourth, after the salt).
Several brands now on the market fill this requirement.  Avoid solid
margarines, solid cooking fats of any kind (natural or not) and butter.

                                    Steve Harris, M.D.

From: B. Harris)
Subject: Re: Butter vs Margarine
Date: Tue, 02 Dec 1997

In <65vl0f$> (Keith Lynch) writes:

>In article <65v8v0$>,
>Steven B. Harris <> wrote:
>> And liquid margarines with next to no hydrogenated fats in them,
>> aren't bad for you at all.  They're equivalent to polyunsaturated
>> fat oils.
>I thought all fats promote obesity, cancer, and diabetes, even if
>some don't also promote atherosclerosis and heart disease.

   There's a threshold effect in polyunsaturate fat cancer promotion in
animal studies.  As for calories, a calorie is a calorie.

>And doesn't peanut oil promote atherosclerosis and heart disease
>even though it's neither saturated nor trans?

   Yes, but that's a specific effect of peanut oil, and has nothing to
do with the fatty acids involved.  Instead, it has to do with the ORDER
they occur on the glycerine backbone.  For some reason, the peanut
order is atherogenic.  Change the order, and it isn't.  This doesn't
happen with other oils, BTW.

> (Are any liquid
>margarines made with peanut oil?)

   None that I know of.  Corn and soybean oil I've seen.  If you find a
peanut one, stay away from it.

                                        Steve Harris, M.D.

From: B. Harris)
Subject: Re: hydrogentated oil
Date: 18 Jan 1998 08:02:59 GMT

In <> "Syd Baumel" <>

>>    As for effects on health, the jury is still out.  For every
>>chicken little saying that margarine kills 10s of thousands a
>>year, there is somebody more rationally pointing out that we
>>think this mainly because of epidemiologic studies showing that
>>margarine eaters die more often of heart disease.  But what's the
>>first thing doctors for the last 20 years have done with people
>>at risk for heart disease, or who have it?  Yep, put them on
>>margarine.  The correlation may well be the other way.  Perhaps
>>heart disease causes margarine.  The data don't exclude that.
>Here's at least one well-pedigreed study that does. It suggests that in
>aging men without CHD, each additional daily tsp of old-fashioned, trans-
>FA- rich margarine eventually increases the risk of CHD by 10%:
>Epidemiology 1997 Mar;8(2):144-149 Margarine intake and subsequent
>coronary heart disease in men.
>Gillman MW, Cupples LA, Gagnon D, Millen BE, Ellison RC, Castelli WP
>Margarine is a major source of trans fatty acids, the intake of which has
>risen since the early 20th century. Some data indicate that consumption
>of trans fatty acids increases the risk of coronary heart disease (CHD).
>In 1966- 1969, 832 men from the Framingham Study, age 45-64 years and
>free of CHD, were administered a single 24-hour dietary recall, from
>which we estimated total daily margarine intake. We calculated CHD
>cumulative incidence rates and, using proportional hazards regression,
>CHD incidence rate ratios over 21 years of follow-up. Mean energy intake
>was 2,619 kcal; mean margarine intake was 1.8 (range 0-12) tsp per day.
>There were 267 incident cases of CHD. Age- adjusted CHD cumulative
>incidence rose over categories of margarine intake, but the increased
>risk was apparent only in the second half of the follow-up period.
>Adjusted for age and energy intake, the risk ratio for CHD for each
>increment of 1 teaspoon per day of margarine was 0.98 [95% confidence
>interval (CI) = 0.91-1.05] for the first 10 years of follow-up and 1.10
>(95% CI = 1.04- 1.17) for follow-up years 11-21. Adjustment for total fat
>intake and for cigarette smoking, glucose intolerance, left ventricular
>hypertrophy, body mass index, blood pressure, physical activity, and
>alcohol intake did not materially change the results. Butter intake did
>not predict CHD incidence. These data offer modest support to the
>hypothesis that margarine intake increases the risk of coronary heart
>  Comment in: Epidemiology 1997 Mar;8(2):122-3
>PMID: 9229205, UI: 97373152

   Comment: that's an interesting study, but still doesn't explain why
the men who were eating more margarine were eating more margarine.
They must have had a reason.  High cholesterol?  There were
(apparently) free of CAD, but were they free of a family history of
CAD?  Does everybody who switches to margarine do so because of overt
evidence of heart disease?  I don't think so.

    Overall, it's a small association, and it's not very convincing.
Indeed, the lack of the expected association of CAD development with
butter intake suggests that some confounding variable is opperating to
have more people at lower risk eating butter at the outset, and those
at higher risk eating margarine, even before the MIs start.  Don't
laugh at the idea.  What did YOU eat?  Is taste all you go by?  Have
YOU had an MI or evidence of CAD?

                                             Steve Harris, M.D.

From: B. Harris)
Subject: Re: Elevated Triglycerides and HDL ratio (EPA in Cultured Salmon)
Date: 29 Jan 1998 23:47:55 GMT

In <>
(Alf Christophersen) writes:

> (NLW TFW NM) wrote:
>>Re:"The problem with much of the salmon in US markets is that it is
>>farmed and therefore lacks EPA. ... So, eat farmed salom and avoid
>>possible PCBs and take fish oil to supply the EPA."
>>Here I thought I was doing SO well eating a slab of (farm, I presume)
>>salmon each week.
>Norwegian farmed salmon is fed a diet giving it even more EPA than
>normal for the wild salmon.
>So maybe here is a good reason to have the government open the gate for
>importing Norwegian salmon??
>By the way, I do not believe that american farmed salmon lack EPA
>either. I think it is rather a rumour put out by some wild salmon
>catchers :-)


   Absolutely.  Sears also is out to lunch on that.  While it is true
that fish eating EPA and DHA in plankton have more of these in their
fat (just as humans who eat these in the diet have more), these
FFAs are too useful to be essential in the diet in either fish or
humans.  Mammals and fish in general have elongases and delta-5
and delta-6 desaturases, allowing them to make at least some DHA
and EPA if the diet has any omega-3 source, as for example the
alpha linolenate/ ALA (18:3n-3) which is present (though in lower
amounts) in corn oil.  The only thing you can say about wild-
caught fish, vs. cultured fish getting corn is that the wild fish
will have less EPA (and less n-3 FFAs in general), not that
they'll have *none.*

   Here's an abstract showing that salmon have the proper
desaturases to make long chain PUFAs from ALA, just as (BTW) you
do.  Of course, in humans it takes a little art to really get
these working maximally, starting from shorter chain FFAs.
However, by cutting down your total fat consumption (to free up
your enzymes from various n-6 conversions) and taking an ALA
supplement (1 or 2 tablespoons of linseed oil a day) you can
raise your DHA and EPA levels about as much as if you were eating
a lot of cold water fish.  Whether or not salmon themselves could
do the same is something I don't know, but my bet is that they
can at least make as much EPA and DHA as they need for their
thermal environment.  Remember, young salmon spend a lot of time
in cold fresh water where they get no plankton at all.  If they
couldn't make 20:5n-3 and 22:6n-3 from 18:3n-3 they'd be up the
creek without an enzyme.

                              Steve Harris, M.D.

Lipids 1997 Dec;32(12):1237-1247
Fatty acyl desaturation in isolated hepatocytes from Atlantic
salmon (Salmo salar): stimulation by dietary borage oil
containing gamma-linolenic acid.

Tocher DR, Bell JG, Dick JR, Sargent JR

NERC Unit of Aquatic Biochemistry, Department of Biological and
Molecular Sciences, University of Stirling, Scotland.

[Medline record in process]

The effects of different dietary oils on the fatty acid
compositions of liver phospholipids and the desaturation and
elongation or [1-14C]18:3n-3 and [1-14C]18:2n-6 were investigated
in isolated hepatocytes from Atlantic salmon. Atlantic salmon
smolts were fed diets containing either a standard fish oil
(FO) as a control diet, a 1:1 blend of Southern Hemisphere marine
oil and tuna orbital oil (MO/TO), sunflower oil (SO), borage oil
(BO), or olive oil (OO) for 12 wk. The SO and BO diets
significantly increased the percentages of 18:2n-6, 18:3n-6,
20:2n-6, 20:3n-6, and total n-6 polyunsaturated fatty acids
(PUFA) in salmon liver lipids in comparison with the FO diet. The
BO diet also increased the percentage of 20:4n-6. Both the SO and
BO diets significantly reduced the percentages of all n-3 PUFA in
comparison with the FO diet. The OO diet significantly increased
the percentages of 18:1n-3, 18:2n-6, total monoenes, and total
n-6 PUFA in liver lipids compared to the FO diet, and the
percentages of all n-3 PUFA were significantly reduced. With
[1-14C]18:3n-3, the recovery of radioactivity in the products of
delta 6 desaturation was significantly greater in the hepatocytes
from salmon fed SO, BO, and OO in comparison with the FO diet.
The BO diet also increased the recovery of radioactivity in the
products of delta 5 desaturation. Only the BO diet significantly
affected the desaturation of [1-14C]18:2n-6, increasing recovery
of radioactivity in both delta 6- and delta 5-desaturation
products. In conclusion, dietary BO, enriched in gamma-linolenic
acid (18:3n-6), significantly increased the proportions of both
20:3n-6 and 20:4n-6 in salmon liver phospholipids and also
significantly increased the desaturation of both 18:2n-6 and
18:3n-3 in salmon hepatocytes. The possible relationships between
dietary fatty acid composition, tissue phospholipid fatty acid
composition, and desaturation/elongation activities are

From: B. Harris)
Subject: Re: Omega-3 and Omega-6 Fatty Acids
Date: 10 Mar 1998 22:37:52 GMT

In <> "Chris Mangum"
<> writes:

>I have read that long-term supplementation with Omega-3 rich oils (flax)
>can deplete the body of Omega-6 fatty acids. Is there a test to determine
>the levels of these fatty acids in the body? If so, what are the
>preferred levels for optimum health?

   You get way too much omega 6 in any reasonable diet (even Pritikin)
to be in danger of depletion of that.  Too much flax (omega-3) probably
can oxidize you, however, if you take too much.  It's the stuff in
paint thinner, you know, and the process that causes the stuff to
spontaneously combust also goes on slowly in your fat stores.  After a
while, your fat turns into fibrous yellow, oxidized gunk!  Or, at
least, this is what happens in pigs when fed too much linseed oil.
Pigs have a digestive system much like that of humans, and my guess is
you don't want to eat what is bad for pigs, at the very least.

   Keep it to less than one teaspoon of flax oil a day, unless you
really have a need to rev up the omega 3 pathways (some kind of chronic
inflammatory disease).  And even then, it's probably best to keep to
less than two tablespoons a day.  Use very fresh oil out of a
refrigerated small black plastic bottle with a recent back-date.  Get a
brand that is bottled under nitrogen, and which smells and tastes good.
Don't store it (even refrigerated) after opening, more than a week or
two, and add some d-alpha tocopherol from a capsule when you open the
bottle.  And remember to take your vitamin E in doses of at least 400
IU a day.

                                          Steve Harris, M.D.

From: B. Harris)
Subject: Re: Omega-3 and Omega-6 Fatty Acids
Date: 11 Mar 1998 04:26:15 GMT

In <> Marconi <> writes:

>I appreciate the insight on flax oil. The only question I have is
>whether the tablespoon/day suggestion is dependent on the type of
>lifestyle. For example, would a person who lives a sedentary lifestyle
>consume the same amount as one who works out on a regular basis. I am a
>ectomorph (6' 1" 175 lbs) who works out regularly in a somewhat feable
>attempt to gain some muscle. I figured the extra calories from several
>tablespoons could only help me. Am I way off base?

    Yah.  If you're into oil for the calories, for heaven sake do
something neutral which won't oxidize you or raise your cholesterol too
much.  Like almond oil.  Tastes better, too.  For calories without too
many other nutritional drawbacks I personally recommend almond butter
and huckleberry jelly sandwiches on whole wheat.  You might as well
enjoy that weight gain.

                                            Steve Harris, M.D.

From: B. Harris)
Subject: Re: Fats that Heal, Fatheads that Kill  (was: Before I spend a
Date: 29 Mar 1998 23:06:16 GMT

In <> Tom Matthews <> writes:

>> far, for his prejudice and crusade against omega-6 fats shows up
>> in bizarre ways everywhere.
>Steve, this doesn't jibe with his "Perfect Oil Blend" product (which I
>use) which contains 22% omega-6.

    I should've been more clear.  Look, I didn't mean that he
recommends no omega-6, as it's obviously an EFA (I'll abbreviate
omega-6 as n-6).  The prejudice against n-6 I'm talking
about is basically that Erasmus recommends lower n-6/n-3 ratios
than are found in most diets, and lower than can be supported by
solid research as being optimal (not enough research exists at
this point to say what is optimal!)  It's a sort of religious
fervor with him.  And it's okay with me if Erasmus plugs n-3's
but not if it gets to the point that he becomes completely blind
to n-3 contents that don't pass his inspection.

   >>Steve, I haven't read Urasmus' book and I am not going to
question your judgement of the other things you note in this
message, but I have consulted several tables concerning the
omega-3 content of corn oil, specifically of alpha linolenic acid
and they all say that it does have 1% or less (some even list it
as zero).<<

   Well, it's not zero-- it's roughly 0.7%.  And what the value
actually is, is important, because the requirements for n-3 in
mammals are very, very low, particularly in adults.  Three ounces
of corn oil a day will supply the adult daily requirement of n-3
(which is in the neighborhood of 0.5 g to 0.75 g per day), even
though corn oil is a poor source of n-3 compared with many other
oils.  (For reference, the typical US diet supplies about 1 gram
of ALA a day, and the Canadian diet about twice that, due to

  >> It may well be enough to keep your lab mice well (possibly
because mice are naturally true vegetarians and don't have as
much need for omega-3 fatty accids as humans do), <<

   Nonsense!  Stop with such blather-- it's me, remember?  Mice
are fond of insects, and are as much omnivores as humans are.
Furthermore, if anything, the normal diet of field mice "in the
field" is far higher in seeds, grains, and PUFAs than that of the
average primate in the field (high caloric density is critical
for mice with their surface to volume ratio).  If you could "dope
out" what the EFA requirements of rodents vs. primates "should"
be, from the composition of their natural diets, you'd expect
rodents to need far MORE EFAs.

   Of course, in biology it's never safe to do that (as I keep
telling you).  In actual fact, since all EFAs can be synthesized
to some extent in the body, causing requirements for them to be
conditional and not absolute, it's been very hard to pin down n-3
"needs" in mammals.  Certainly, they vary widely depending on
stage of life, conditions, etc (the n-3/n-6 ratio, for example,
is much more important in growth phase than in adulthood).  In
humans, textbook recommendation for adult n-3 intake is 0.2% to
0.3% energy as n-3, and clinical n-3 deficiency in adult humans
has not, to my knowledge, been described at n-3 intakes above
0.1% total energy.  That represents about 0.25 gram of n-3 per
day, and is practically impossible to go below, on any kind of
normal mixed diet.  Clinically, it's seen in brain-damaged people
being tube fed with the old unbalanced diets (not anything you
can get in a can today!), or in patients getting the old low fat
TPN by IV.

   >>but I do not think that this particular critcism of Udo
Erasmus is justified.<<

    Certainly it is.  The man doesn't know what he's talking
about, is all.  If you read him, you're going to get a very
unbalanced picture of how modern nutrition regards EFAs.

  >>Not only is it not likely to be optimal, but since corn oil
also contains 13% saturated fat, such a ratio implies as I stated
above that the value is close to 1% or less and that many tables
will quite reasonably list it as *zero*.<<

   But it's NOT reasonable to list it as zero, if you're thinking
nutritionally.  As well list the vitamin B content of flour as
zero, since it's also less than 1% by weight.  And again, the
point was not just that tables list it as zero, but that Erasmus
says flatly that corn oil has no ALA in it.  My point is that not
only it *have* ALA in it, but that corn oil has *nutritionally
significant* amounts of ALA in it (for mice and humans alike),
and Erasmus should have known better.  But since he's got his
blinders on, I suppose he somehow doesn't see the n-3 in corn
oil.  It's rather as if Linus Pauling had written that orange
juice doesn't have any vitamin C in it.  You could make excuses
for him, saying that it's a small amount by weight, or because
the amounts are trivial compared with what Pauling thinks is
optimal for people-- but none of this would really fly because
there's no excuse for this sort of thing from somebody who claims
to be a nutritionist, or to being giving you the latest in
nutritional thinking.  You don't get to just dismiss nutrient
contents completely and pretend they don't exist, if they don't
come up to what your pet theories demand.

   >>Again maybe such a small amount of linolenic acid is
sufficient for mice and other vegetarian lab animals, but this
does not imply that it is sufficient for more omnivarous

   Everything we know about the human need for n-3 suggests that
the amount in corn oil is more than enough to prevent any n-3
deficiency syndrome ever described, if corn oil makes up any
significant fraction of dietary calories (like more than 15% of
calories).  Whether or not the levels of n-3 you can get from
reasonable amounts of corn oil used as sole fat source, are
*optimal* in terms of other health parameters (cancer prevention,
say) is an interesting question, and one worthy of discussion.  I
never said it wasn't.  If Erasmus had simply said that corn oil
when used as major fat source has enough n-3 to prevent the n-3
clinical deficiency syndrome, but not enough for best health or
best longevity, and then presented the evidence for *that,* I'd
have no quarrel with him.

                                      Steve Harris

Can J Physiol Pharmacol 1996 Jun;74(6):629-639
The Canadian Society for Nutritional Sciences 1995 Young
Scientist Award Lecture. Recent studies on the synthesis,
beta-oxidation, and deficiency of linoleate and alpha-linolenate:
are essential fatty acids more aptly named indispensable or
conditionally dispensable fatty acids?

Cunnane SC

Department of Nutritional Sciences, Faculty of Medicine,
University of Toronto, ON, Canada.

Recent research on the synthesis, beta-oxidation, and deficiency
of linoleate and alpha-linolenate raises questions about whether
the term essential fatty acid is outdated. Linoleate and alpha-
-linolenate can be synthesized from their respective 16-carbon
precursors, which are present in the human diet; whether
the rate of conversion and dietary supply of the precursors are
sufficient depends on the actual requirement for linoleate and
alpha-linolenate. Pure deficiency of linoleate (diet excluding
linoleate but including alpha-linolenate and oleate) has not been
studied until recently, so it is unclear whether the recommended
linoleate intake at 2% of energy, as based on classical essential
fatty acid deficiency studies, is appropriate or too high.
Despite marked whole-body depletion of linoleate and poor
conservation of linoleate stores, pure linoleate deficiency has
little effect on growth in rats, suggesting its requirement may
be less than 2% of energy. Whole-body fatty acid balance studies
indicate that the main route of linoleate and alpha-linolenate
metabolism is oxidation, which increases sufficiently that
accumulation of dietary linoleate and alpha-linolenate may
actually be prevented in undernutrition and fasting refeeding.
Part of the oxidized carbon from linoleate and alpha-linolenate
is recycled and used for de novo synthesis of "non-essential"
fatty acids and cholesterol, which in the brain of the
suckling rat, can exceed conversion to longer chain polyunsatura-
tes by as much as 10- to 40-fold. Given the capability to
synthesize linoleate and alpha-linolenate, the imprecise
knowledge of true linoleate requirement, and the absence of clear
symptoms of their deficiency in healthy adults, it might
be advantageous to consider using the terms indispensable and
conditionally dispensable to clarify the conditional nature of
the dietary requirement for linoleate and alpha-linolenate.

Publication Types:
  Review, tutorial

And since you don't like mouse data, here's a paper on n-3
deficiency in humans.

J Intern Med Suppl 1989;225(731):171-175
n-3 fatty acid deficiency in man.

Bjerve KS

Department of Clinical Chemistry, Regional Hospital, University
of Trondheim,

A total of nine patients with n-3 fatty acid deficiency are
described. They had been fed by gastric tube for 2.5-12 years,
and had received 0.02-0.09% of calories as n-3 acids. The
observed clinical symptoms of n-3 fatty acid deficiency were
scaly and haemorrhagic dermatitis, haemorrhagic folliculitis of
the scalp, growth retardation and impaired wound healing. All
patients had extensive brain damage making it impossible to
evaluate n-3 effects on cerebral functions. The patients were
supplemented with cod liver and soya oil, alpha-linolenate
followed by a purified fish oil, or with a mixture of linseed
and cod liver oil. The results indicate that a dietary supply of
1.0-1.2% of alpha-linolenic acid is necessary to obtain a
mid-normal lipid concentration of n-3 fatty acids, and suggest
that the minimal dietary requirement is 0.2-0.3% of total calori-
es. Long-chain n-3 fatty acids seem to be approximately twice as
efficient as alpha-linolenic acid in maintaining normal n-3 fatty
acid concentrations in plasma and red cell lipids.

From: B. Harris)
Subject: Re: Fats that Heal, Fatheads that Kill  (was: Before I spend a
Date: 30 Mar 1998 05:38:14 GMT

In <> "Syd Baumel" <>

   >>Let's put it this way: If you're trying to keep your dietary
intake of pure fats and oils to a minimum -- as virtually every
health authority, orthodox and alternative, recommends -- you
will get vanishingly little omega-3 bang for your buck out of
corn oil.<<

    Yes, but nobody eats a diet like that.  You'd have to be
doing something really crazy and dumb like following the Pritikin
10% fat restriction, AND avoiding whole vegetables and grains--
instead making your own semi-synthetic AND low fat diet out of
pure casein, carbohydrate, and... corn oil.  Which is, BTW,
precisely how the early cases of EFA deficiency in people on
semi-sythetic "tube feeding" happened (they were low fat mixes,
and all the fat was corn oil or milk fat).  It's practically
impossible to see clinical EFA deficiency any other way.  In any
kind of actual Pritikin style diet using a reasonable mix of
whole foods, you would certainly get a better n-6/n-3 ratio than
is available in corn (such diets use almost no oils as isolated
oils, of course).  As for my rodents, they did fine because they
were run at at least 30% of calories as corn oil.  Had I run them
at 10% calories as fat, and used corn oil, I might have had

   >>  But if -- against all sensible dietary
counsel -- you're willing to invest 15-30% of your caloric intake
in it, this will still, at best, ensure that you have only a
theoretically "adequate" intake of ALA, albeit along with a
disproportionate abundance of linoleic acid which will compete
very aggressively with the scarce ALA molecules for the
enzyme that converts them to their respective longer-chain EFAs
and eicosanoids.  So why tempt fate? <<

    No reason.  And I don't think it's crazy to supplement a gram
or two of alpha-linolenate a day, just to make sure you're more
than topped off on n-3 EFAs (this is certainly cheap and easy to
do, as that amounts to just a teaspoon of linseed or a tablespoon
of Canola).  However, at the same time I can also point out that
the average person, even somebody on a Pritikin program, is far
less likely to be marginal on n-3 fatty acids than they are for a
dozen other nutrients.  It's not the same situation, in other
words, that we know goes on for iron, magnesium, folate, B6, and
so on and so on, where less than RDA intakes are very widespread.
In that sense, yes-- I do think that Udo Erasmus' book promotes a
certain hysteria over something that is WAY down the list of
nutritional things to get concerned about.

  >>It's impressive, though, that your rats did so well on a corn
oil diet, Steve.  I wonder if -- to the extent that they're more
vegetarian than us -- they're genetically adapted to synthesize
long-chain omega-3's much more efficiently than us, in which case
they would be more tolerant of the omega-3 limitations of such a
diet than we would be.<<

   As I remarked to Tom, I don't think that lab rodents are more
naturally vegetarian than humans.  They're omnivores and show
typically omnivore behavior.  If you stress lab rodents, for
instance, they eat their young like pigs do.  And the males kill
what are likely to be the young of other males, much as happens
with chimps and lions.  When did you last hear of that happening
with cows or sheep?  As a matter of fact, I can tell you that if
you calorie-restrict mice and don't cage them separately, they
canibalize each other in adulthood quite as readily as they do
their litters.  That will never happen with rabbits.

   Again, mice in the wild subsist on a fairly high fat diet--
they need the calories of such a diet to keep warm (and their
arteries and lipid-handling systems show that high tolerance for
fat).  The natural intake of PUFAs and EFAs of a wild mouse, as a
fraction of calories, must be substantial.  This differs by
species, of course, and Onychomys spp (grasshopper or scorpion
mice), which eat almost entirely insects, will be eating fewer
PUFAs than Mus spp or a species like the cotton mouse, Peromyscus
gossypinus, which eats a lot of cotton seeds.  But I can't think
of any reason why any of these rodents should be better at making
n-3's than humans are, or at making the very long n-3's either.
So far as I can tell, herbivores have roughly the same EFA
requirements as omnivores.  It is only full carnivores like cats
that have odd requirements.

   As for needing more very long chain n-3s in the cold, that may
be true if you're a fish, and have to keep your fat at a very
cold ambient temp.  So far as I know, though, it doesn't hold
true for homeotherms.

                                  Steve Harris, M.D.

P.S.  We live in too septic a society probably.  The average
person used to have an innate understanding of the carnivorous
proclivities of rodents.  Have you never read _1984_?  How about
"The Pit and the Pendulum"?

From: B. Harris)
Subject: Re: Fats that Heal, Fatheads that Kill  (was: Before I spend a
Date: 30 Mar 1998 13:06:38 GMT

In <> Tom Matthews <> writes:

>BTW, here is a quote from the supposedly authoritative _Present
>Knowledge in Nutrition_ 7th ed page 60: "In contrast, corn, sunflower,
>and safflower oils all contain very low amounts of 18:3n-3 (<1% fatty
>acids), and when fed as the single dietary source of polyunsaturated
>fat, these oils result in n-3 fatty acid defeciency."

    While strictly true, also misleading.  Feeding as "the single
dietary source of polyunsaturated fat" is not the same as feeding a
given oil as the single dietary source of fat, period.  In the bad old
days people got milk fat in their tube feedings, and only corn oil for
their "polyunsaturated fat" requirements (a tablespoon a day or so).
As everyone has noted, they did poorly.

>Chapter 7 titled _Essential Dietary Lipids_ containing page 60 was
>written by Sheila Innis, PhD, Department of Pediatrics, University of
>British Columbia.
>She goes on to say "A dietary intake of 0.5-1.0% of energy from
18:3n-3 gives maximum tissue levels of 22:6n-3 and also avoids any
apparent deficiency symptoms." <

   So it does.  And so does a lot less (avoid deficiency symptoms).  As
for levels of 22:6-n3 (DHA) these levels are not simply a matter of ALA
to energy ratio (as the quote implies), but more a function of n-3/n-6
ratio since (as discussed) the two classes of EFA compete for the same
elongase enzymes in going from 18 carbons to longer chains.  It's also
(as I noted) far more difficult keeping DHA levels up in infants and
children than in adults, and as Dr. Innis is a pediatrician, it might
be worth checking her references to see who she's talking about in that
quote.  Pediatricians get up-tight about DHA, since it's the main EFA
needed for growth in the CNS.  I noted that.  Dispite what a
pediatrician thinks, it's far from clear that the goal in adults is to
simple-mindedly get as much n-3 into the tissues as possible (how
Denham Harman would choke at that, since HE thinks free radicals from
DHA are responsible for Alzheimer's disease...).  Again, n-3 and n-6
EFAs have very different effects on the prostaglandin pathways and
which you want more of might well depend on what you plan to be doing.
If you plan to be fighting infections and wounds, I suspect you're
going to want less n-3s.  If you're at risk for atherosclerosis and
thrombosis, you may want more.  Unfortunately, as with aspirin,
nobody is really sure of what the optimum is, and exactly for whom.
Like the optimal dose of vitamin C, the optimum n-3/n-6 ratio is one of
those things that must be decided by experiment and epidemiology, and
can't be figured out from first principles, however much we'd like to.

   As for my other comment, I didn't mean to sound snooty, and I
promise to let you tell me about mouse nutrition right after you let me
lecture you about the ins and outs of busted hard drive data recovery.

                                      Steve Harris, M.D.

From: B. Harris)
Subject: Re: Canola Oil and Trans Fatty Acids
Date: 14 Apr 1998 23:38:52 GMT

In <> (Paul) writes:

>I read in 'Alive' magazine that you shouldn't cook with Canola oil
because the heating process converts the omega-3 fatty acids into
dangerous trans fatty acids.  Is this an accurate statement, and if so,
would using colp pressed Extra Virgin Olive oil be a better (safer?)
oil to cook with?<

   If by "cook" you mean fry, there is some truth in this.  The 10%
omega-3 alpha-linolenic acid in Canola does both oxidize and racemerize
(turn partly to trans-FFA) when you heat it to high temps (frying
temps).  Alpha-linolenic acid is particularly susceptable to that.  I
know that hit men from Canada are on their way to my home even as I
write these words, yet I cannot tell a lie.  Monounsaturated oils with
low polyunsaturate content, like olive, almond, walnut, and avocado are
much better for frying and broiling.  For ordinary cooking in cakes and
casseroles where temps don't get much over 150 F, most any oil is okay,
though monos are still in theory better.  Canola (so long as it's
unhydrogenated) is handy because it supplies your RDA of omega-3 fats
easily (2 teaspoons a day more than does it).  And it also has a high
monounsaturated content, which is good for your cholesterol.  But use
it on salads.  Again, if you heat oils, try to make them
monounsaturated ones.

   It is possible to buy hydrogenated Canola, which is theoretically
okay for frying because it has little omega 3 in it.  But it's hard to
be sure if the hydrogenation has been done in the cold European style
(which results in fewer trans fatty acids), or at higher temps, which
result in the trans fatty acids you're trying to avoid.  And, of
course, you don't get the health benefits of the omega-3's either.  I'd
probably stay away from the stuff, therefore.

                                         Steve Harris, M.D.

From: B. Harris)
Subject: Re: Article on Canola Oil
Date: 30 Aug 1998 20:23:10 GMT

In <uk9G1.4646$Z_4.6338548@tor-nn1-ca> "David Lloyd-Jones"
<> writes:

>Rapeseed being renamed canola cannot help but remind one of the immortal
>words of Lyndon Johnson as he signed the Auto Pact: "Well, here come the
>Canadians fucking us in the ear again".

   Rapeseed wasn't just "renamed" Canola, like Chinese gooseberries
were renamed Kiwi-fruit.   Canola has been bred to produce much less
erucic acid than the rapeseed or Colza oil long used in Europe.  This
is the stuff which is cardiotoxic in rodents, and maybe (nobody is
sure) in people.  Erucic is also a major component of "Lorenzo's Oil",
if you ever saw that movie.  There was big discussion in there about
whether or not the rodent data applies to humans.  My guess is that in
standard salad oil doses, it makes no difference.

                                          Steve Harris, M.D.

From: B. Harris)
Subject: Re: cholesterol too low
Date: 20 Dec 1998 06:56:37 GMT

In <> Bill Ellis Fleenor
<> writes:

>Richard J. Marsico wrote:
>> In October of this year I had some blood work done.  Triglycerides came
>> in at 588 with total cholesterol being 274.  I'm 41 years of age and
>> have been lifting weights for eleven years (no aerobics).  Acting on
>> these results, I switched to a low fat diet and started some regular
>> aerobic work.  One month ago my readings came in at 488 for tri's and
>> total cholesterol was down to 174.  Yesterday I god my latest results.
>> Triglycerides are now 351 with total cholesterol being 131 (ldl is 30
>> and hdl is 31).  I now find out that total cholesterol should not
>> be below 160!  How does one find a happy medium without driving oneself
>> nuts????!!!!
>> I also take 800 i.u. of E, 1000mg of C, and 50mg of q10 daily at my
>> doctor's request.  Any suggestions would be very much appreciated.
>> Rick
>Triglycerides of 351 are too high. Here's a link:
>Conventionally, triglycerides are not considered elevated
> unless they are greater than 150 or even 200 mg/dL.
>Elevated triglycerides can be caused by diet (fatty foods,
>sweets, fruit juices, and alcohol can all increase levels)
>as well as by genetic factors. Most people can reduce their
>triglyceride levels significantly through exercise and
>a low-fat, low-sugar diet although some people with very
>high levels may need medication.
>Editorial Comment:
>The debate about the importance of triglycerides in predicting
> heart disease risk continues and is certainly not settled by
> these two studies. Nevertheless, they provide additional
> information: we should pay attention to our triglyceride
> levels. What's the bottom line? Cholesterol is still the
> major factor to pay attention to, and of course the
> breakdown to LDL and HDL cholesterol is very important.
> However, once that information is known, the person with higher
> triglycerides is probably at higher risk than the one with lower
> triglycerides for a given level of LDL cholesterol. Treatment
> with medication remains focused mostly on LDL cholesterol unless
>the triglycerides are over about 500 mg/dL. Remember, triglycerides
> are greatly affected by the last meal and therefore should only
> be measured after a 12-hour overnight fast. "
>Copyright ©1996-1998 Center for Cardiovascular Education, Inc.,
> New Providence, NJ USA. All rights reserved.
>x-posted to

    A second editorial comment:  There is certainly one more thing to
try before medication, especially if you've got your cholesterol where
you want it.  Fish oil is effective at lowering trigylcerides at doses
of 10-20 g a day (10-20 capsules of 1 gram each).  That's fish body
oil, as fish *liver* oil (ie, codliver oil) in such doses has too much
vitamin A in it.  (If it doesn't say codliver, you're probably okay).
If you don't mind swallowing that many pills over a day, you can
probably try this route for less than the drug price, if you buy fish
(body) oil from a deep discount place like COSTCO.

   That much fat is only about 100-200 extra Calories a day, and should
not affect your weight much.  Nor your cholesterol, since it's highly
unsaturated.   Your skin may become a lot more oily, and you won't like
the taste of your belches.  Otherwise, fish oil is pretty benign.  The
biggest risk is that it's about as anti-platelet as aspirin, so people
with histories of bleeding stroke GI bleeding, or uncontrolled high
blood pressure in the recent past, probably shouldn't take fish oil.
And the combination of fish oil and aspirin may be synergistic, so if
you take aspirin you might consider stopping.

     If you must try a drug, atorvastatin ("Lipitor") is particularly
good at lowering triglycerides at even low doses (5 mg a day or less).
I suggest buying the high dose pills (20 mg) and cutting them in
quarters, to start.  That will save quite a lot of money.  You'll need
a doc for the Rx and to help you monitor your liver for toxicity signs
for the first while you're on it.

                                   Steve Harris, M.D.

From: B. Harris)
Subject: Re: Omega-3 fatty acids: cancer promoter or preventer?
Date: 2 Mar 1999 08:30:47 GMT

In <> "physical (Droll Troll)"
<> writes:

>The solution to this would appear to be fish farms. HPLC-mass spec would
>answer this definitively. There should be articles on this, as well as
>the stability of these oils on storage.

    The articles on fish farms are rather funny.  I mentioned that cold
water fish get a lot of omega 3 fats from the fish they eat, which get
it in turn ultimately from cold water plankton.  Plus, I suspect that
cold itself stimulates fish to make more omega-3's. In fish farms they
feed them corn meal in warmer water, and the result is much lower omega
3 levels than in wild fish.

>  Gel caps
>make me sick to my stomach, even with food.  I suspect that color is a
>good indicator of freshness, but I could be wrong.

    Since I'm starting to see completely black flax capsules, that
would be a problem...

>	Oh, and just a reminder, Brian, that Arachidonic acid is linoleic
>_sparing_, not strictly substitutive. :)

    News to me.  Is there something important that linoleic acid does
in the body besides make arachadonate??  So what if you can't make 1
series prostaglandins-- are there any you really need?  And (provided
you're not a cat) doesn't the synthetic enzyme work "backwards" as well
to make linoleate from arachadonate anyway, so you can eat either one?

From: B. Harris)
Subject: Re: Omega-3 fatty acids: cancer promoter or preventer?
Date: 3 Mar 1999 12:38:05 GMT

In <>
(Alf Christophersen) writes:
> B. Harris) wrote:
>>>	Oh, and just a reminder, Brian, that Arachidonic acid is linoleic
>>>_sparing_, not strictly substitutive. :)
>>    News to me.  Is there something important that linoleic acid does
>>in the body besides make arachadonate??  So what if you can't make 1
>>series prostaglandins-- are there any you really need?  And (provided
>>you're not a cat) doesn't the synthetic enzyme work "backwards" as well
>>to make linoleate from arachadonate anyway, so you can eat either one?
>Linoleate makes their own variants by cyclooxygenases and lipoxygenases.
>The cyclooxygenases has been reported to have the opposite effect as the
>PG-2 series (the products are the C18-analogues of PG's)

    Yes.  So what?  Again-- if the effect big enough to see clinically?
 And can't you make linoleic from arachadonate anyway?

From: B. Harris)
Subject: Re: Omega-3 fatty acids: cancer promoter or preventer?
Date: 4 Mar 1999 09:28:18 GMT

In <>
(Alf Christophersen) writes:

> B. Harris) wrote:
>>    Yes.  So what?  Again-- if the effect big enough to see clinically?
>> And can't you make linoleic from arachadonate anyway?
>Arachidonate are probably made more to C22:5(n-6) and C22:6(n-6) than
>backwards to linoleate via all shortening and saturations.

   Yes, but so WHAT?  We seem to be having a failure to communicate.
What evidence do you have that humans need series 1 prostagladins AT
ALL?  Any more than cats do?  Even if the worst scenario were true and
we can't convert arachadonate to linoleate at all (which cats can't,
but I suspect humans can, since they have the enzyme for the forward
process)?  If you want to argue that some dietary linoleate is
absolutely necessary for humans, you've got to provide evidence for
both claims.  I frankly don't believe it.  We know it's perfectly
possible for humans to get along, reproduce, live normally, on a diet
of almost nothing but meat (Esquimos), very much like cats.   If
linoleate were absolutely essential for people, that would be a pretty
difficult trick.

From: B. Harris)
Subject: Re: Omega-3 fatty acids: cancer promoter or preventer?
Date: 5 Mar 1999 13:41:20 GMT

In <7blrkf$t8l$> (Nimrod Gil-Ad)

>C22:6(n-6)?  I.e. 6,9,12,15,18,21cisC22:6??
>I thought the delta-21 bond is the one that connects to the carboxyl,
>which means it can't be desaturated.  Am I wrong?

   No, you're right.  C22:6(n-3) is the familiar DHA.  There is no
C22:6:n-6, for reasons you note.

From: B. Harris)
Subject: Re: Flax seed oil capsules
Date: 5 Mar 1999 14:39:26 GMT

In <> (Polar)

>	The bottle I purchased says "1 to 9 capsules per day"
>???  That's a pretty wide variation.
>	Any feedback on which is optimum?  I have nothing wrong except
>acid stomach (hiatal hernia w/reflux); otherwise pretty good health,
>	You input appreciated.

   Americans get about a gram of ALA a day, Candians 2 grams (Canola).
The stuff is 50% ALA, about, so you're talking 2 or 3 to double your
American intake to get to the Canadian intake.  And you go on from

From: B. Harris)
Subject: Re: Fish oil
Date: 19 Mar 1999 11:34:28 GMT

In <> Brian Manning Delaney
<> writes:

>> It is not the animals fault that they contain so
>> much omega-6 compared to omega-3, but the
>> farmers who want to decrease amount of money
>> spent on feeding their animals to increase profit.
>Yup. They should get some kind of fee or kickback from the
>supplement companies who capitalize on this change in n-3
>content of food by pushing DHA and EPA pills. The supplement
>companies, should, in turn, get a kickback from the people who
>profit from the increased Usenet and Web traffic resulting
>from the spreading of bogus health needs ("MAKE MONEY FAST!").
>And since agribusiness uses software and computers from some
>of these companies for crop-planting, -fertilizing, etc.
>purposes, the circle is complete. A little greed goes a long
>way. The perpetual motion of the free market. God, life is

   To be fair, farmers would be fools not to raise what people want to
buy.  You can raise hogs on flax, but they get a funny yellow fat
disease.  You can raise them fishoil and even cornoil, and the bacon
then comes out fishy tasting, or at the very least, looking slimey like
something left out in the warm too long.

   It's true, as a snack foods lobbyist once said to a congressional
committee, that people want to see healthier foods in vending machines
and behind the glass in delis.  But the problem is they just want to
SEE them in there.  They don't actually want to buy and EAT them.

From: "Steve Harris" <>
Subject: Re: Is it possible to have too little sugar in your diet?
Date: Tue, 15 May 2001 13:21:22 -0700

Here's a nice review for you all. It's not a simple as saying
that all fat is bad, and in particular there is evidence that
omega-3 fats improve glucose tolerance.  Alas, the high
fat intake types sometimes don't do it the way the
Eskimos do.

There are also other odd epidemiological trends. Fat
does not come out to be the villain in every single
vascular event, but rather just the ones influenced
by classical atherosclerosis. Ischemic stroke risk,
for instance tends to be DECREASED by both
saturated and monounsaturated fat intake in the
epidemiological analysis, but is not affected by
polyunsaturate intake (go figure).

That's if you control for other factors. One would expect
that the vegans might have nice clean arteries and
great cholesterols, but stroke out anyway. However,
a vegan diet is so high in potassium and such a
great treatment for high blood pressure, that
the relationship of diet to stroke may not be so
clear over all.

Looking over all of this, my general impression
is that the epidemiology still supports a modified
Pritikin approach. Which is to say, Pritikin plus
some foods that Pritikin wouldn't have approved,
in large quantity, like fish, fancy nuts, eggs, olives,
avocados, etc.

Atherosclerosis 2000 Jun;150(2):227-43

Relationship of dietary fat to glucose metabolism.

Lichtenstein AH, Schwab US

Lipid Metabolism Laboratory, Jean Mayer USDA Human Nutrition Research
Center on Aging at Tufts University, 711 Washington St., 02111, Boston,

The relationship between dietary fat and glucose metabolism has been
recognized for at least 60 years. In experimental animals, high fat diets
result in impaired glucose tolerance. This impairment is associated with
decreased basal and insulin-stimulated glucose metabolism. Impaired
insulin binding and/or glucose transporters has been related to changes
in the fatty acid composition of the membrane induced by dietary fat
modification. In humans, high-fat diets, independent of fatty acid
profile, have been reported to result in decreased insulin sensitivity.
Saturated fat, relative to monounsaturated and polyunsaturated fat,
appears to be more deleterious with respect to fat-induced insulin
insensitivity. Some of the adverse effects induced by fat feeding can be
ameliorated with omega-3 fatty acid. Epidemiological data in humans
suggest that subjects with higher intakes of fat are more prone to
develop disturbances in glucose metabolism, type 2 diabetes or impaired
glucose tolerance, than subjects with lower intakes of fat.
Inconsistencies in the data may be attributable to clustering of high
intakes of dietary fat (especially animal fat) with obesity and
inactivity. Metabolic studies suggest that higher-fat diets containing a
higher proportion of unsaturated fat result in better measures of glucose
metabolism than high-carbohydrate diet. Clearly, the area of dietary fat
and glucose metabolism has yet to be fully elucidated.

Publication Types:
Review, academic

From: "Steve Harris" <>
Subject: Re: Lecithin for cholesterol
Date: Tue, 5 Mar 2002 18:50:21 -0800
Message-ID: <a6403n$v7p$>

gary wrote in message ...
>Consider Lecithin with phosphatydlcholine for improving cholesterol.  Three
>1200 mg per day for about three weeks saw a high cholesterol client go from
>250 to 170 in less than a month.  She was also on a multi that is rich in
>Bs, and I had her on flax-seed oil and soy protein Jamba-style smoothies.
>Lecithin is part of my regular list to advocate for several things,
>including cholesterol.

Lecithin has been looked at as a cholesterol lowering agent, and it's no
better than an equal weight the polyunsaturated fat which it contains. Which
raises two problems:

1) Lecithin is a lot more expensive than polyunsaturated oil (corn oil or
safflower), and
2) In the Wadsworth VA studies where polyunsaturated oil was deliberately
used to lower cholesterol, they had fewer heart attacks but more GI cancer,
and gained nothing in life span. This is consistant with animal studies.
Polyunsaturated fat loading is probably not the optimal dietary way of
lowering cholesterol.


From: Steve Harris <>
Subject: Re: high cholesterol and use of flax seeds or other foods
Date: 20 Jun 2005 10:52:55 -0700
Message-ID: <>

>>Thanks to generous subsidies to EU growers, this is now one of the
cheapest and most widespread vegetable oils. In general, if an oil is
made from anything other than canola / rapeseed, this will be stated on
the label.  Beware of oil simply described as "vegetable oil" - it will
invariably be made from canola / rapeseed. <<


In Canada maybe, but not in the USA!  *Here* the designation means that
it is invariably soybean oil.


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