From: sbharris@ix.netcom.com(Steven B. Harris)
Newsgroups: sci.med.nutrition
Subject: Re: Evening Primrose Oil v Fish oil v Flaxseed Oil?
Date: 17 Feb 1999 04:54:42 GMT

In <36c9b0a8.19444114@nntp.uio.no> alf.christophersen@basalmed.uio.no
(Alf Christophersen) writes:
>
>kstuart@jps.net (Ken Stuart) wrote:
>
>>Thus, the best way to avoid modern health problems is to avoid farm
>>products. Since this is difficult to do, best is to avoid farm products
>>that don't occur in the wild (in an easily edible form), such as grains,
>>that cause hyperinsulinemia, and to supplement all those substances that
>>were plentiful in the hunter/gatherer diet, but not in the modern diet,
>>including EPA and minerals.



    Look, this is a ridiculous argument.  There is nothing unchangeable
about your DHA and EPA levels, even if you don't eat any.  The lower
the amount of saturated fat you get, the more EPA and DHA you make out
of the ALA in your diet (fats compete for elongases).  With a good low
fat diet, even if you eat no fish or game meat at all, you will have
tissue levels of DHA and EPA comparable to those of animals in the
wild.  Some of whom, after all, are vegetarians also.

    Vegans do NOT have low levels of EPA and DHA.  It's been measured.
They do considerably better than the rest of this high sat fat society,
even if it does eat a little fish now and then.

                                  Steve Harris, M.D.

From: sbharris@ix.netcom.com(Steven B. Harris)
Newsgroups: sci.med.nutrition
Subject: Re: Evening Primrose Oil v Fish oil v Flaxseed Oil?
Date: 18 Feb 1999 05:47:20 GMT

In <36CA8694.6EC5@netcom.ca> Tom Matthews <tmatth@netcom.ca> writes:

>Steven B. Harris wrote:
>>
>>     Look, this is a ridiculous argument. There is nothing unchangeable
>> about your DHA and EPA levels, even if you don't eat any. The lower the
>> amount of saturated fat you get, the more EPA and DHA you make out of
>> the ALA in your diet (fats compete for elongases). With a good low fat
>> diet, even if you eat no fish or game meat at all, you will have tissue
>> levels of DHA and EPA comparable to those of animals in the wild. Some
>> of whom, after all, are vegetarians also.
>>     
>>     Vegans do NOT have low levels of EPA and DHA. It's been measured.
>> They do considerably better than the rest of this high sat fat society,
>> even if it does eat a little fish now and then.
>
>This is all quite true indeed.
>I was not trying to make any claim that vegetarians did *not* have
>reasonable amounts of omega-3's in their *system*, but only that they
>might have more (and more easily obtained) and thus be even healthier
>than they usually already are, if they also ate a little fish or fish
>oil.
>
>And BTW, in my book any dietary practice which is not *optimal* for
>health and longevity is ipso facto *dangerous* to ones health. Or at
>least it will be seen as such when one dies earlier than one might have
>otherwise done.


     We didn't evolve from fish-eating monkeys, Tom.  Or even from
primates that ate a lot of game meat (though they did canibalize each
other, occasionally).  I suppose it's possible that we don't make
enough DHA and EPA for our healthy old age (since evolution's not too
interested in that), but I doubt it.  We are able to make a lot.

   The main reason for this seems to be that the growing infant in the
first 2 years needs a LOT of DHA for the structure of the developing
brain, and the infant and the mother have to make most of that, out of
what they get in the diet, which usually does not include much
pre-formed DHA (and didn't, for most of our evolutionary history).
And since evolution certainly IS interested in the intelligence and
brain development of young fruit-eating primates, it seems quite
unlikely that it would have shorted them on optimal activity of an
enzyme they already have to make something which is often in short
supply in the diet they evolved on.  So I rather think enough capacity
is there for ALA--> optimal DHA, in a low saturated fat diet.  I can't
prove it, but I sure don't worry much at night that it might not be
true.  There are, IMHO, far more likely nasty possible nutritional
problems for the average person eating the average American diet.

    It's always possible to argue that we're not eating the OPTIMAL
amount of any of the zillion biochemicals we're made out of, and are
capable of absorbing and using, if we ate them.  But it's just not cost
or time efficient to worry about more than a few of the most likely
ones.
                                        Steve Harris, M.D.

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.cardiology,misc.health.alternative,sci.med.nutrition
Subject: Re: Study: Broil or bake fish for heart benefits
Date: 6 May 2005 14:08:46 -0700
Message-ID: <1115413726.421444.251880@f14g2000cwb.googlegroups.com>

>>It's funny that people like yourself can see the nonsense involved in
much of "nutritional science" today, but yet you don't realize that
there is absolutely no scientific evidence that dietary polyunsaturated
fatty acids are needed by non-pregnant, adult humans (humans can and do
make their own PUFA, called the Mead acid, which is very stable and yet
does everything the omega 3s and 6s can do). <<


COMMENT:
That is complete nonsense. Read a modern textbook. You can't even grow
mammalian cells in a dish without lipids. If you try, they accumulate
"Mead's acid" (aka ETA or 18:3w9) which they synthesize, and die. Of
essential fatty acid deficiency. I'll append an abstract at the end of
this, and you can find it on medline and click on the links to find
dozens of cases of EFA deficiency in culture. As well as the use of
Mead's acid to diagnose the condition in vivo as well. And interesting
preliminary work that w-9 ETA makes cancer cells grow faster, and w-3
EFAs slow it down. The kinds of things made from w-9 fats are
pathological in many systems. Why you think they might substitute for
w-3 in your brain is beyond me. It's well known that mammals have no
systems to make w-3 or w-6 fatty acids from w-9's like ETA.

There are numerous examples known of essential fatty acid deficiency in
human adults. And experimentally in many other mammals besides rodents.


>> The study that is quoted
(there is only one) as a citation that "proves" the "essentiality" of
omega 3 and 6 PUFAs was done in 1930 on rats.<<

No. Read a modern text book.


>>I can't
prove that dietary PUFAs are not essential, but I've avoided them for a
few years now and feel better than ever.<<


COMMENT:
It's pretty hard to avoid them completely. And on a low level, you
really don't know what your coronaries are doing, or what cancers
you're encouraging.


>>  My grandparents never had any  appreciable source of omega 3s and
still don't, yet are doing fairly well (early 90s, mid 80s).<<


COMMENT:
Your grandparents never ate plants, or animal that eat plants?
Remarkable. They must still be on hyperalimentation, or eating a
semisynthetic diet of hydrogenated cocoanut oil.


>>  If anyone wants to take me up on the offer,
I'll put up a huge amount of money (and you match it) - loser pays for
the experiment and admits defeat in a signed and notarized document,
given to the winner.  We will feed one group of dogs no appreciable
source of fat except for cocount oil, and the other group gets plenty
of omega 3s and 6s, and if the coconut dog group lives significantly
less then you win, but if not, then I win. I choose what to feed the
dogs on the coconut oil diet, in terms of non-fat items - you can feed
your unfortunate dogs the same, as long as they are getting a few grams
of omega 3s and 6s each day. <<


COMMENT:

You'll no doubt have one sick group of dogs.  Dogs fed only
hydrogenated coconut oil (to remove all PUFAs) with cholesterol (which
dogs normally handle well) actually get atherosclerosis (!) which is
quite remarkable for dogs. And it's prevented by adding just a little
high omega-6 and omega-3 PUFA plant oil. See the abstract below. Your
experiment has already been done for you, essentially. Do you want to
send me a check for pointing this out?



>>Have you ever realized that there is no standard for the amount of
"essential fatty acids" people are supposed to consume each day, unlike
other essential nutrients? <<


COMMENT:
These things all have standard intake ranges to prevent deficiency.
Have you ever read a modern nutrition textbook in your life?  The
chapters on fats have references, you know. Start with Goodhart and
Shils.

 >>There is a huge scientific literature documenting how dangerous
PUFAs can be (especially of the omega 3 and 6 variety).<<


COMMENT:
No, sorry, but the longest lived populations in the world (Japanese and
Icelanders) have some of the highest omega-3 intakes.  Omega-6 intakes
are a mixed back due to the pro-inflammatory nature of arachadonate (as
you mention), but even that can be avoided by cutting down on meat
intake, and using plant-based omega-6 precursors (like GLA) to
encourage pathways away from arachadonate.

>> One researcher commented that it appears that arachidonic acid is not
safe at any level and in any tissue.  Several have ommented about how
these fatty acids appear to be the root cause of most "chronic
disease."<<

COMMENT:
They should tell that to the Japanese and the Icelanders.

>>  The
papers are being published at a nearly daily rate.  Just go to
pubmed.com and search for arachidonic, lipid peroxidation, linoleic,
oxidative stress, and reactive oxygen species, for example, if you
think I am fabricating this.<<

COMMENT:
No, I can see them. But these papers are wonderful examples of theory
trying to trump facts.  Life span feeding studies in rodents at least
show that high PUFA diets are not harmful so long as various other
vitamins and minerals (like vitamin E and Se) are not in short supply.


>> If we are not to pay attention to the
many researchers who have come to this conclusion, why should we listen
to any scientist?  How can we accept one terribly flawed study from
1930 and yet ignore hundreds that have been published recently?  Why
not just create a religion of food?  Oh, I forgot, that's the situation
that we are presently in now. <<

COMMENT:

Nonsense. See the following two abstracts, and see the references for
the first one.

Proc Natl Acad Sci U S A. 1995 Feb 14;92(4):1147-51.

Development and characterization of essential fatty acid deficiency in
human endothelial cells in culture.

Lerner R, Lindstrom P, Berg A, Johansson E, Rosendahl K, Palmblad J.

Department of Medicine, Karolinska Institute, Stockholm Soder Hospital,
Sweden.

We induced an essential fatty acid deficiency (EFAD) in human umbilical
vein endothelial cells by culture in medium with 20% (vol/vol)
delipidated fetal calf serum. EFAD, reflected by decreased cellular
linoleic acid (18:2 omega 6) and arachidonic acid (20:4 omega 6) and
emergence of the oleic acid derivative 5,8,11-eicosatrienoic acid (20:3
omega 9; Mead's acid), was evident after 1 week of culture and became
pronounced after 2 weeks. Beyond that time point, control cells (cultured
in 20% normal fetal calf serum) grew deficient of 18:2 omega 6, and EFAD
cells died. 18:2 omega 6 addition to EFAD cells resulted in
dose-dependent increases of 18:2 omega 6 and 20:4 omega 6. 20:4 omega 6
or 5,8,11,14,17-eicosapentaenoic acid (20:5 omega 3) additions resulted
in normalization of these acids, and conversion of 20:5 omega 3 to
4,7,10,13,16,19-docosahexaenoic acid (22:6 omega 3) was noted.
Agonist-induced increases in concentrations of prostacycline
(prostaglandin I2; PGI2) and cytosolic Ca2+, [Ca2+]i, were reduced in
EFAD cells and not restored by 18:2 omega 6 or 20:4 omega 6 additions.
Change of the medium in EFAD cultures 1 day before the experiments
decreased 20:3 omega 9 and normalized the PGI2 production and [Ca2+]i
changes, whereas addition of 20:3 omega 9 to control cells impaired the
[Ca2+]i response, indicating a suppressive effect of 20:3 omega 9.  Thus,
EFAD in endothelial cells is associated with abnormalities of eicosanoid
and second-messenger production partly attributable to 20:3 omega 9
accumulation.  Moreover, the gradual emergence of 18:2 omega 6 deficiency
in regularly grown control cells underlines the need for careful analysis
of fatty acids in long-term cell cultures.

PMID: 7862650 [PubMed - indexed for MEDLINE]


===================================
Lab Invest. 1976 Apr;34(4):394-405.

Experimental canine atherosclerosis and its prevention. The dietary
induction of severe coronary, cerebral, aortic, and iliac atherosclerosis
and its prevention by safflower oil.

McCullagh KG, Ehrhart A, Butkus A.

Severe atherosclerotic lesions were produced without thyroid suppression
in seven out of eight dogs by feeding semisynthetic diets containing 5
per cent cholesterol and 16 per cent hydrogenated coconut oil for 12 to
14 months.  Occlusive plaques were located in the coronary arteries and
major cerebral arteries as well as in the aorta and iliac vessels. The
lesions were characterized by an intense sclerotic reaction to areas of
lipid deposition and foam cell accumulation in the intima. The diet
induced a rapid elevation of plasma-free and esterfied cholesterol,
triglyceride, and phospholipid, and the extent of aortic atherosclerosis
was shown to be partially dependent on mean plasma cholesterol
concentration. A second group of eight dogs were fed a diet identical
with the first except for the replacement of 4 per cent hydrogenated
coconut oil by 4 per cent safflower oil. Despite receiving the same
amounts of dietary cholesterol and fat, this second group of dogs was
completely protected from the atherogenic process. Plasma lipids became
only slightly elevated and no induced atherosclerotic lesions were found
at autopsy. Circulating thyroid hormone concentrations were similar
between the two groups of dogs and the thyroid glands had a normal
morphology in both groups.

PMID: 1263442 [PubMed - indexed for MEDLINE]

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition
Subject: Re: Not too little omega 3s, but too much omega 6s.
Date: 28 May 2005 20:08:58 -0700
Message-ID: <1117336138.599961.258670@g49g2000cwa.googlegroups.com>

>>Here's just another example of what I've been saying here for years
now.  At least these researchers are honest enough to admit what their
experiment revealed, unlike so many others who begin with assumptions
about how very dangerous fatty acids are "essential" to humans when one
rat experiment was done in 1929/30 (Burr & Burr), before all essential
nutrients, such as some of the B vitamins, were known, and thus any
experiment done at that time would have to be done again with all the
known nutrients, controlling for what is being tested for essentiality
(plus, dogs would be better than rats for this experiment - much closer
to humans in terms of fatty acid metabolization). <<


COMMENT:

A lot of experimental evidence has demonstrated the need of n-3 and n-6
EFAs in the diet of both young and old mammals since 1930. You seem to
be having difficulty either finding it or retaining it.  Perhaps a
shortage of n-3 in your own brain?

SBH

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition
Subject: Re: Not too little omega 3s, but too much omega 6s.
Date: 28 May 2005 20:10:34 -0700
Message-ID: <1117336234.570665.240450@g43g2000cwa.googlegroups.com>

Br J Nutr. 2000 Dec;84(6):803-12.

The conditional nature of the dietary need for polyunsaturates: a
proposal to reclassify 'essential fatty acids' as
'conditionally-indispensable' or 'conditionally-dispensable' fatty acids.

Cunnane SC.

Department of Nutritional Sciences, Faculty of Medicine, University of
Toronto, Canada. cunnane@utoronto.ca.

The term essential fatty acid no longer clearly identifies the fatty
acids it was originally used to describe. It would be more informative if
the concept of essentiality shifted away from the symptoms arising from
the lack of de novo synthesis of linoleate or alpha-linolenate and
towards the adequacy of the capacity for synthesis and conservation of
both the parent and the derived long-chain polyunsaturates. For instance,
despite the existence of the pathway for synthesis of docosahexaenoate
from alpha-linolenate, the former would be more correctly classified as
'conditionally indispensable' because the capacity of the pathway appears
insufficient during early development, although it may be sufficient
later in life in healthy individuals. Similarly, despite the inability to
synthesize linoleate de novo, abundant linoleate stores and its
relatively slow turnover in healthy adults probably makes linoleate
'conditionally dispensable' for long periods. There are two other
anomalies with the terms essential and non-essential fatty acids: (1)
under several different experimental circumstances, the C-skeleton of
essential fatty acids is avidly used in the synthesis of non-essential
fatty acids; (2) to function normally, the brain is required to
endogenously synthesize several non-essential fatty acids. As with
essential amino acids, which have been reclassified as indispensable or
conditionally indispensable, such a change in terminology should lead to
an improved understanding of the function and metabolism of
polyunsaturates in particular, and long-chain fatty acids in general.

Publication Types:
    Review
    Review, Tutorial

PMID: 11177196 [PubMed - indexed for MEDLINE]



J Nutr Health Aging. 2004;8(3):163-74.

Roles of unsaturated fatty acids (especially omega-3 fatty acids) in the
brain at various ages and during ageing.

Bourre JM.

INSERM Research Director. Unit U26 Neuro-pharmaco-nutrition. Hopital
Fernand Widal, 200 rue du Faubourg Saint Denis. 75745 Paris cedex 10.
jean-marie.bourre@fwidal.inserm.fr

Among various organs, in the brain, the fatty acids most extensively
studied are omega-3 fatty acids. Alpha-linolenic acid (18:3omega3)
deficiency alters the structure and function of membranes and induces
minor cerebral dysfunctions, as demonstrated in animal models and
subsequently in human infants. Even though the brain is materially an
organ like any other, that is to say elaborated from substances present
in the diet (sometimes exclusively), for long it was not accepted that
food can have an influence on brain structure, and thus on its function.
Lipids, and especially omega-3 fatty acids, provided the first coherent
experimental demonstration of the effect of diet (nutrients) on the
structure and function of the brain. In fact the brain, after adipose
tissue, is the organ richest in lipids, whose only role is to participate
in membrane structure. First it was shown that the differentiation and
functioning of cultured brain cells requires not only alpha-linolenic
acid (the major component of the omega-3, omega3 family), but also the
very long omega-3 and omega-6 carbon chains (1). It was then demonstrated
that alpha-linolenic acid deficiency alters the course of brain
development, perturbs the composition and physicochemical properties of
brain cell membranes, neurones, oligodendrocytes, and astrocytes (2).This
leads to physicochemical modifications, induces biochemical and
physiological perturbations, and results in neurosensory and behavioural
upset (3). Consequently, the nature of polyunsaturated fatty acids (in
particular omega-3) present in formula milks for infants (premature and
term) conditions the visual and cerebral abilities, including
intellectual.  Moreover, dietary omega-3 fatty acids are certainly
involved in the prevention of some aspects of cardiovascular disease
(including at the level of cerebral vascularization), and in some
neuropsychiatric disorders, particularly depression, as well as in
dementia, notably Alzheimer's disease. Recent results have shown that
dietary alpha-linolenic acid deficiency induces more marked abnormalities
in certain cerebral structures than in others, as the frontal cortex and
pituitary gland are more severely affected. These selective lesions are
accompanied by behavioural disorders more particularly affecting certain
tests (habituation, adaptation to new situations). Biochemical and
behavioural abnormalities are partially reversed by a dietary
phospholipid supplement, especially omega-3-rich egg yolk extracts or pig
brain. A dose-effect study showed that animal phospholipids are more
effective than plant phospholipids to reverse the consequences of
alpha-linolenic acid deficiency, partly because they provide very long
preformed chains. Alpha-linolenic acid deficiency decreases the
perception of pleasure, by slightly altering the efficacy of sensory
organs and by affecting certain cerebral structures. Age-related
impairment of hearing, vision and smell is due to both decreased efficacy
of the parts of the brain concerned and disorders of sensory receptors,
particularly of the inner ear or retina. For example, a given level of
perception of a sweet taste requires a larger quantity of sugar in
subjects with alpha-linolenic acid deficiency. In view of occidental
eating habits, as omega-6 fatty acid deficiency has never been observed,
its impact on the brain has not been studied. In contrast, omega-9 fatty
acid deficiency, specifically oleic acid deficiency, induces a reduction
of this fatty acid in many tissues, except the brain (but the sciatic
nerve is affected). This fatty acid is therefore not synthesized in
sufficient quantities, at least during pregnancy-lactation, implying a
need for dietary intake. It must be remembered that organization of the
neurons is almost complete several weeks before birth, and that these
neurons remain for the subject's life time. Consequently, any disturbance
of these neurons, an alteration of their connections, and impaired
turnover of their constituents at any stage of life, will tend to
accelerate ageing. The enzymatic activities of sytivities of synthesis of
long-chain polyunsaturated fatty acids from linoleic and alpha-linolenic
acids are very limited in the brain: this organ therefore depends on an
exogenous supply. Consequently, fatty acids that are essential for the
brain are arachidonic acid and cervonic acid, derived from the diet,
unless they are synthesized by the liver from linoleic acid and
alpha-linolenic acid.  The age-related reduction of hepatic desaturase
activities (which participate in the synthesis of long chains, together
with elongases) can impair turnover of cerebral membranes. In many
structures, especially in the frontal cortex, a reduction of cervonic and
arachidonic acids is observed during ageing, predominantly associated
with a reduction of phosphatidylethanolamines (mainly in the form of
plasmalogens). Peroxisomal oxidation of polyunsaturated fatty acids
decreases in the brain during ageing, participating in decreased turnover
of membrane fatty acids, which are also less effectively protected
against peroxidation by free radicals.

Publication Types:
    Review
    Review, Tutorial

PMID: 15129302 [PubMed - indexed for MEDLINE]



J Nutr. 1998 Feb;128(2 Suppl):427S-433S.

Comment in:
    J Nutr. 1999 Feb;129(2):446.

The slow discovery of the importance of omega 3 essential fatty acids in
human health.

Holman RT.

Hormel Institute, University of Minnesota, Austin 55912, USA.

Although linoleic and linolenic acids have been known to be necessary for
normal growth and dermal function since 1930, the omega 3 essential fatty
acids (EFA) have not received much attention until recently. The two
families of acids are metabolized by the same enzymes, making them
competitive. Gross deficiencies of omega 6 plus omega 3 EFA have been
observed in humans, induced by attempts at total parenteral nutrition
(TPN) with preparations devoid of lipids.  Deficiency of omega 3 acids
has been induced by TPN containing high omega 6 and low omega 3 fatty
acids. In natural human populations, a wide range of omega 3 and omega 6
proportions have been found, ranging from high omega 3 and low omega 6
content to low omega 3 and high omega 6 content, showing inverse
correlation between sigma omega 6 and sigma omega 3. In humans with
neuropathy or impairment of the immune system, significant deficits of
omega 3 EFA have been measured.

Publication Types:
    Review
    Review, Tutorial

PMID: 9478042 [PubMed - indexed for MEDLINE]




Curr Opin Clin Nutr Metab Care. 2002 Mar;5(2):127-32.

Efficiency of conversion of alpha-linolenic acid to long chain n-3 fatty
acids in man.

Brenna JT.

Division of Nutritional Sciences, Savage Hall, Cornell University,
Ithaca, New York 14853, USA. jtb4@cornell.edu

Alpha-linolenic acid (18:3n-3) is the major n-3 (omega 3) fatty acid in
the human diet. It is derived mainly from terrestrial plant consumption
and it has long been thought that its major biochemical role is as the
principal precursor for long chain polyunsaturated fatty acids, of which
eicosapentaenoic (20:5n-3) and docosahexaenoic acid (22:6n-3) are the
most prevalent. For infants, n-3 long chain polyunsaturated fatty acids
are required for rapid growth of neural tissue in the perinatal period
and a nutritional supply is particularly important for development of
premature infants. For adults, n-3 long chain polyunsaturated fatty acid
supplementation is implicated in improving a wide range of clinical
pathologies involving cardiac, kidney, and neural tissues. Studies
generally agree that whole body conversion of 18:3n-3 to 22:6n-3 is below
5% in humans, and depends on the concentration of n-6 fatty acids and
long chain polyunsaturated fatty acids in the diet. Complete oxidation of
dietary 18:3n-3 to CO2 accounts for about 25% of 18:3n-3 in the first 24
h, reaching 60% by 7 days. Much of the remaining 18:3n-3 serves as a
source of acetate for synthesis of saturates and monounsaturates, with
very little stored as 18:3n-3.  In term and preterm infants, studies show
wide variability in the plasma kinetics of 13C n-3 long chain
polyunsaturated fatty acids after 13C-18:3n-3 dosing, suggesting wide
variability among human infants in the development of biosynthetic
capability to convert 18:3n-3 to 22:6n3. Tracer studies show that humans
of all ages can perform the conversion of 18:3n-3 to 22:6n3. Further
studies are required to establish quantitatively the partitioning of
dietary 18:3n-3 among metabolic pathways and the influence of other
dietary components and of physiological states on these processes.

Publication Types:
    Review
    Review, Tutorial

PMID: 11844977 [PubMed - indexed for MEDLINE]





Annu Rev Nutr. 2004;24:597-615.

Dietary n-6 and n-3 fatty acid balance and cardiovascular health.

Wijendran V, Hayes KC.

Foster Biomedical Research Lab, Brandeis University, Waltham,
Massachusetts 02254, USA. vwijen@brandeis.edu

Epidemiological and clinical studies have established that the n-6 fatty
acid, linoleic acid (LA), and the n-3 fatty acids, linolenic acid (LNA),
eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) collectively
protect against coronary heart disease (CHD). LA is the major dietary
fatty acid regulating low-density lipoprotein (LDL)-C metabolism by
downregulating LDL-C production and enhancing its clearance. Further, the
available mass of LA is a critical factor determining the hyperlipemic
effects of other dietary fat components, such as saturated and trans
fatty acids, as well as cholesterol. By contrast, n-3 fatty acids,
especially EPA and DHA, are potent antiarryhthmic agents. EPA and DHA
also improve vascular endothelial function and help lower blood pressure,
platelet sensitivity, and the serum triglyceride level.  The distinct
functions of these two families make the balance between dietary n-6 and
n-3 fatty acids an important consideration influencing cardiovascular
health. Based on published literature describing practical dietary
intakes, we suggest that consumption of ~6% en LA, 0.75% en LNA, and
0.25% en EPA + DHA represents adequate and achievable intakes for most
healthy adults.  This corresponds to an n-6/n-3 ratio of ~6:1. However,
the absolute mass of essential fatty acids consumed, rather than their
n-6/n-3 ratio, should be the first consideration when contemplating
lifelong dietary habits affecting cardiovascular benefit from their
intake.

Publication Types:
    Review

PMID: 15189133 [PubMed - indexed for MEDLINE]

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition
Subject: Re: Linoleic acid a carcinogen?
Date: 18 Jun 2005 23:11:04 -0700
Message-ID: <1119161464.196194.174760@g47g2000cwa.googlegroups.com>

>>There are several studies showing
that people or animals with Mead acid instead of omega 6
polyunsaturates in their tissues have lower inflammation or are more
resistant to it, which makes sense biochemically. <<

COMMNENT

Studies on what species of animal?  The studies which suggest that
PUFAs, especially LA (linoleic acid 18:2w-6) are "carcinogenic", are
likely to be based on rodent work. Rodents are great at converting this
to GLA, DHGLA, and finally to arachadonate (AA = 20:4w-6), which as you
out point out below is a big inflammatory. And is probably what gives
rodents on high PUFA diets cancer (though there is a threshold effect
for PUFA dose and cancer in mice and rats, and it is NOT the case that
the less PUFA in rodent diet the better, as you seem to imply).

Humans, however, don't convert LA to GLA very well, and since GLA is
rare in the diet, humans eating large amounts of LA don't seem to
suffer from too much arachadonate (AA) as rodents do. As with cats and
other carnivores, most AA in humans is eaten in the human diet,
pre-formed. We get it from eggs and turkey and bacon grease and milk
and stuff like that. And all that AA may well be part of what's giving
us more cancer on the Western diet. Vegans who get no pre-formed AA and
a LOT of plant LA, don't have big inflammatory problems, or cancer
problems. Sorry, but that's an epidemiological fact. We're not big
rodents.

People who bypass the desaturase block from LA to GLA by taking GLA
supplements directly (EPO, blackcurrent, borage) without an EPA w-3
supplement to block the conversion of GLA to AA in the liver, get a big
AA blast they surely aren't looking for.  But they're rare. Anybody
taking borage these days is probably also taking fishoil.


>>If you do a search for arachidonic depression on sciencedaily.com
you'll see that the levels of this horribly damaging substance are
elevated in depressed patients brains, and there is something called
arachidonic cascade mania, another biochemical situation that leads to
psychological disorders. <<

COMMENT:

Fine. Have them eat less eggs and poultry. Also farmed salmon seems
amazingly high in AA, since fish also are great at making it from LA
(which they get in their corn feed when aquacultured).

>>Indeed, the so-called epidemic of autism is
likely due to the much higher intake of linoleic acid now, as compared
to 30 or so years ago.  It wouldn't take much to test this idea, and
pleny of scientists are writing about it, but the big healthy agencies
are usually looking for bacteria, viruses, high cholesterol, or
something else that is either irrelevant or a secondary phenomenon. <<

COMMENT:
They're looking for mercury. Forgetting that the first big push in
MMR/thimerosal vaccination happened in the middle 60's. All our
autistics in the US should be about > 40-45 years old right now.  Which
is not what we observe.

Anyway, autism is not more common in big LA eaters. Autistic Jains?
Autistic Adventists? No, I don't think so.

Again, humans aren't rats or fish. We don't turn LA into AA that
efficiently. Which means LA is not the pro-inflammatory for us that it
is for these other species. I know you want to eat hydrogenated coconut
oil and don't want to hear this either, but that's too bad. WIthout
some LA, you're one day going to wind up like the hydrogenated coconut
fed dogs.

SBH

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition
Subject: Re: Montygram: Fish oils (Omega-3) do not promote harmful peroxidation
Date: 23 Aug 2005 16:42:46 -0700
Message-ID: <1124840566.869347.317960@z14g2000cwz.googlegroups.com>

montygram wrote:
> Your attempts to discredit me will only work on those who are very
> stupid.  If you know of an experiment that verified the 1930 Burr &
> Burr one, then you should post it.  Otherwise, that is the only
> experiment that has been done that is on point.  I have researched all
> the studies in the major nutrition textbooks, and they all refer to the
> same one.  You are the one stuck in 1930, MMu, not me.
>
> If you can propose another animal model other than dogs that would be
> less expensive, let's talk.  The animal would have to be one that does
> not continue to grow throughout life and also does not eat seeds as
> part of its natural diet.


COMMENT:

Rats grow throughout life, and mice eat seeds, so you've just elimiated
the two most common experimental animals. Cats get essential fatty acid
defficient, but that's because they have no delta-6 desaturase (unlike
humans).

If your hypothesis was correct, adult humans would need NO fat of any
kind in the diet. Since all fats can be synthesised de-novo BUT the
essential ones (which is what makes them essential). And in that case,
adult humans would do just fine on hyperalimentation in which they got
only sugar, protein, vitamins and minerals.  But that is NOT the case!

They tried this, and humans got skin diseases which responded only to
omega-3 and omega-6 fatty acid supplementation. Your experiment has
been done with people, which are all that matters. We need these
things.

Look at the references in the following article "The slow discovery of
the importance of omega 3 essential fatty acids in human health." Full
text is available online. Read the whole thing and educate yourself.
"Slow Discovery" indeed, since it doesn't include you.

http://www.nutrition.org/cgi/content/full/128/2/427S

J Nutr. 1998 Feb;128(2 Suppl):427S-433S.

Comment in:
    J Nutr. 1999 Feb;129(2):446.

The slow discovery of the importance of omega 3 essential fatty acids
in human health.

Holman RT.

Hormel Institute, University of Minnesota, Austin 55912, USA.

Although linoleic and linolenic acids have been known to be necessary
for normal growth and dermal function since 1930, the omega 3 essential
fatty acids (EFA) have not received much attention until recently. The
two families of acids are metabolized by the same enzymes, making them
competitive. Gross deficiencies of omega 6 plus omega 3 EFA have been
observed in humans, induced by attempts at total parenteral nutrition
(TPN) with preparations devoid of lipids. Deficiency of omega 3 acids
has been induced by TPN containing high omega 6 and low omega 3 fatty
acids. In natural human populations, a wide range of omega 3 and omega
6 proportions have been found, ranging from high omega 3 and low omega
6 content to low omega 3 and high omega 6 content, showing inverse
correlation between sigma omega 6 and sigma omega 3. In humans with
neuropathy or impairment of the immune system, significant deficits of
omega 3 EFA have been measured.

Publication Types:
    Review
    Review, Tutorial

PMID: 9478042 [PubMed - indexed for MEDLINE]

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition
Subject: Re: Montygram: Fish oils (Omega-3) do not promote harmful peroxidation
Date: 23 Aug 2005 19:54:07 -0700
Message-ID: <1124852047.462955.103660@g47g2000cwa.googlegroups.com>

montygram wrote:

> Rats are not a good animal model, nor are cats, but dogs are.  What is
> your point?  I've suggested dogs many times.

I found you a dog experiment and you didn't like it. You won't like any
dog experiment you don't design, and nobody is going to give you
$100,000 to test your silly ideas. Cells from all mammals die in
culture without EFA addition (first making Mead acid in great
abundance). Why would anybody waste any more money killing whole
animals where all mammalian cells die without w-6 and w-3 EFAs?



> Again, Burr used rats,
> which makes no sense if you are going to think about human fatty acid
> needs.  I've already read the literature (mostly Holman's reviews).  Do
> you realize that they compared a no fat diet to one with PUFAs.  They
> didn't use a control diet of fats very low in PUFAs.  That invalidates
> their claims.


Why should it?  The claim is that you need *some* w-3 and w-3 PUFA in
your diet. A zero fat diet should be a perfectly good control, since
you can obviously MAKE any fat you need BUT w-6 and w-3 PUFAs.



> Also, the Mead acid was dicovered later, so they
> couldn't have compared omega 3s and 6s to the Mead acid in 1930 even if
> they wanted to, and they still have not done so to this day!

What do you mean "compared." All w-3 and w-6 deprived animals make mead
acid (w-9), just like dying cells do. So what?


> I would not be surprised if humans were healthier on a diet with a some
> saturated fatty acid content, but since it's nearly impossible to eat a
> totally fat free diet, what is your point?

It's hard to eat a fat free diet,but fat-free total IV nutrition was
the order of the day when it started. It produced results reminiscent
of vitamin deficiency, which were all correctable by w-3 and w-6 EFAs
given IV. These people did not produce Mead acid and do fine. Their
skin started turning into lizzard skin, and they died of infection.


> I've been avoiding omega 3s for about 4 years now and the benefits I've
> seen are incredible.  Exactly when am I supposed to shrivel up and fade
> away (or whatever nonsense "EFAD" is supposed to do)?

You're still getting w-3's (enough to avoid overt deficiency in an
adult) if you're eating any plant fat at all. Probably you aren't
getting enough to avoid coronary disease, but the question when THAT
will kill you is open. If it does, I suppose one day you simply will
stop posting here. But shriveling beforehand is not expected.

If you really want to do an economically possible experiment, why don't
you have your blood omega-3 and omega-6 levels tested directly by a
reputable lab, like Kronos?  Since you obviously can't make them, if
you have any in your blood, it's from your diet (even if you think
you're "avoiding" them.)

BTW, I'm curious as to how you THINK you're avoiding w-3 and w-6 EFAs.
Do you really think coconut oil doesn't contain them? What else do you
eat?

SBH

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition
Subject: Re: Direct Link Between Prostaglandin E2 and Pain Intensity
Date: 28 Aug 2005 10:38:43 -0700
Message-ID: <1125250723.849805.45460@f14g2000cwb.googlegroups.com>

montygram wrote:
> Mr. Cocky seems to enjoy demonstrating his ignorance.  In posts you
> started, I stated that an intelligent person would want Mead acid,
> which is a PUFA the body produces on its own, if not overloaded with
> omega 6 or 3 PUFAs (due to their stronger biochemical activity and
> instability).



COMMENT:

Actually, Mead acid is a poor-substitute w-9 PUFA which the body
produces in desperation when short of w-3/w-6 EFAs, and which cells in
culture produce in large quantity, just before they DIE of w-3 and w-6
deficiency. And ONLY then. The Mead acid doesn't save them (though w-6
and w-3 do, if you add it, following which the Mead acid goes away).
All this reminds me of several of the SOS systems the body uses to try
to repair skin with keratosis and scarring, when deficienct of vitamin
A, or B2. It's a stopgap measure, and ultimately it fails.


> If you want to talk science, fine, that is what this NG
> is for, but don't misrepresent others.  My posts are very clear.  I
> document and explain everything down to the molecular level, sometimes
> even beyond that (for example, I've talked of how the periodic table
> holds useful information to biochemical processes).

COMMENT:
You ignore findings even at the cell level, in culture. Like this one,
which you'll find abundantly documented after a cursory medline search,
and which I've posted reference after ignored reference for you on,
before.

SBH

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition,sci.med,misc.health.alternative
Subject: Re: Deficiency in omega-3 fatty acids tied to ADHD
Date: 5 Sep 2005 23:55:37 -0700
Message-ID: <1125989737.214908.281860@g14g2000cwa.googlegroups.com>

montygram wrote:
> Do you realize that experiments have been done which demonstrate these
> fatty acids to be highly unstable?  I don't know what SBHarris is
> smoking these days, but it must be awfully expensive.  To claim that
> fish oil does not enhance oxidative stress in major ways is worse than
> claiming that the world is flatter than a pancake.  I've read hundreds
> of studies that talk about the susceptibility of double bonds to free
> radical degradation, and it's also basic chemistry.


COMMENT:


Damnit, Monty, actual experiments with living animals trumps anything
you know (or think you know) about basic "theoretical chemistry."
Living systems are always more complicated than you can figure out.
Now, here are those abstracts again. Read and comment on each one, this
time.  Then you can post 12, and I'll do the same for yours. Pay
attension to my asterisks ****


1: Ann Clin Lab Sci. 2005 Spring;35(2):169-73.

Brief communication: omega-3 essential fatty acid supplementation and
erythrocyte oxidant/antioxidant status in rats.

Iraz M, Erdogan H, Ozyurt B, Ozugurlu F, Ozgocmen S, Fadillioglu E.

Department of Pharmacology, Inonu University Faculty of Medicine,
Malatya.
mustafairaz@yahoo.com

Fish oil contains large amounts of essential omega-3 fatty acids, such as
eicosapentaenoic and docosahexaneoic acids, which are building structures
of cell membranes. The goal of this study was to elucidate the effects of
dietary omega-3 fatty acid supplementation on the oxidant/antioxidant
status of erythrocytes in rats. The malondialdehyde (MDA) and nitric
oxide (NO) levels and the catalase (CAT), superoxide dismutase (SOD), and
glutathione peroxidase (GSH-PX) activities were assayed in erythrocytes
of male Wistar albino rats after 30 days of dietary supplementation with
fish oil (0.4 g/kg/day).  Erythrocyte CAT activity in the treated group
was increased in comparison with the control group. Erythrocyte MDA and
NO levels were lower in the treated group than the controls. Erythrocyte
GSH-Px and SOD activities did not differ significantly in the 2 groups.
Negative correlations were found between SOD and CAT activities, and
between SOD and GSH-Px activities in the treated group. In conclusion,
omega-3 fatty acid supplementation helps to prevent lipid peroxidation
and to safeguard erythrocytes from oxidative injury.  Dietary
supplementation with omega-3 fatty acids ***might possibly protect**
tissues from oxygen free radical injury in the various diseases in which
the oxidant/antioxidant defense mechanisms are disturbed.

PMID: 15943181 [PubMed - indexed for MEDLINE]



2: Prostaglandins Leukot Essent Fatty Acids. 2005 Apr;72(4):257-65.

Fish oil before cardiac surgery: neutrophil activation is unaffected but
myocardial damage is moderated.

Charman A, Muriithi EW, Milne E, Wheatley DJ, Armstrong RA, Belcher PR.

Centre for Nutrition & Food Research, Queen Margaret University College,
Edinburgh EH12 8TS, UK.

Could pre-operative dietary intervention with fish oil reduce neutrophil
activation and myocardial damage associated with cardiopulmonary bypass
(CPB)?  Patients were randomised to receive either 8 g/day fish oil
(n=22) or placebo (n=18) for 6 weeks. Neutrophil activation, apoptosis
and cardiac damage were measured. Demographics and operative variables
were similar. Fish oil diet decreased plasma VLDL from 0.69+/-0.34 to
0.51+/-0.24 mmol/l and triglycerides from 1.68+/-0.70 to 1.39+/-0.54
mmol/l. HDL cholesterol increased from 0.94+/-0.27 to 1.03+/-0.26 mmol/l
demonstrating significant treatment effects (P=0.007, 0.02 and 0.0003,
respectively) as well as compliance with treatment.  There were no
significant differences in ex vivo
N-formyl-methionyl-leucyl-phenylalanine-stimulated neutrophil superoxide
anion generation or myeloperoxidase release at recruitment,
pre-operatively and at end-CPB. Apoptosis at end-CPB was equally reduced
in both groups from 23+/-9% to 13+/-4% in the fish oil group (P<0.001)
and 35+/-14% to 15+/-3% in the placebo group (P=0.001). At end-CPB
overall troponin I levels averaged 0.91+/-0.60 ng/ml which clearly
exceeded diagnostic levels (0.15 ng/ml). At 24h troponin I fell
significantly in the fish oil group to 46+/-23% of end-CPB levels
(P=0.0002) whereas it peaked in the placebo group to 107+/-72% (P=0.098
vs.  end-CPB); this difference was significant: P=0.013. At 48 h the
placebo-treated patients had higher troponins but not significantly so
(P=0.059).  Area-under-the-curve analysis did not conclusively support
this (P=0.068). ***We conclude that fish oil did not significantly
decrease post-CPB neutrophil activation (as detected ex vivo) but may
moderate post-operative myocardial damage.***

Publication Types:
    Clinical Trial
    Randomized Controlled Trial

PMID: 15763437 [PubMed - indexed for MEDLINE]



3: Pharmacol Biochem Behav. 2004 Dec;79(4):651-9.

**Protective effect of chronic ethyl docosahexaenoate administration on
brain injury in ischemic gerbils.**

Cao DH, Xu JF, Xue RH, Zheng WF, Liu ZL.

Department of Biology, Nanjing University, 22 Hankou Road, Jiangsu
210093, PR
China.

There is evidence that the excessive generation of reactive oxygen free
radicals contributes to the brain injury associated with cerebral
ischemia. In the present study, the protective effect of chronic
administration of ethyl docosahexaenoate (E-DHA) against oxidative brain
injury was evaluated in the gerbil model of transient cerebral ischemia.
Weanling male gerbils were orally pretreated with either E-DHA (200
mg/kg) or vehicle, once a day, for 10 weeks and subjected to bilateral
occlusion of common carotid arteries for 10 min. At the different
reperfusion times, E-DHA pretreatment significantly inhibited the
increases in the production of brain salicylate-derived
2,5-dihydroxybenzoic acid (2,5-DHBA) and content of brain
malonildialdehyde (MDA). The superoxide dismutase (SOD) activity was not
modified; however, pretreatment with E-DHA significantly prevented the
level of brain-reduced glutathione (GSH) and activities of brain
glutathione peroxidase (GSH-P(X)) and catalase (CAT) from declines caused
by cerebral ischemia. Moreover, ischemia and reperfusion-induced delayed
neuronal loss in the hippocampus CA1 sector and locomotor hyperactivity
were also significantly attenuated by pretreatment with E-DHA. These
results suggested that the neuroprotective effect of E-DHA might be due
to its **antioxidant property.** [Cripes, it's just the ethyl ester of
DHA-- same double bond system]

PMID: 15582673 [PubMed - indexed for MEDLINE]



4: Prog Neuropsychopharmacol Biol Psychiatry. 2004 Jul;28(4):693-8.

Hypothalamic superoxide dismutase, xanthine oxidase, nitric oxide, and
malondialdehyde in rats fed with fish omega-3 fatty acids.

Songur A, Sarsilmaz M, Sogut S, Ozyurt B, Ozyurt H, Zararsiz I,
Turkoglu AO.

Department of Anatomy, Afyon Kocatepe University Medical School,
Turkey.

Phospholipids located in the cellular membrane play a critical role in
the fluid-mosaic model of membrane structure and membrane function.
Evidence is mounting for the role of abnormal phospholipid metabolism in
some neuropsychiatric disorders including schizophrenia. As an important
essential fatty acid (EFA), omega-3 (omega-3) fatty acid series are found
in large amounts in fish oil. The aim of this experimental study was to
assess the changes of some of the oxidant and antioxidant parameters in
the hypothalamus of rats fed with omega-3 EFA diet (0.4 g/kg/day) for 30
days. Eight control rats and nine rats fed with omega-3 were decapitated
under ether anesthesia, and hypothalamus was removed immediately.
Malondialdehyde (MDA) and nitric oxide (NO) levels as well as superoxide
dismutase (SOD) and xanthine oxidase (XO) enzyme activities in the
hypothalamus were measured. SOD activity was significantly decreased in
omega-3 EFA treated group compared to control group (p < 0.014). Tissue
MDA and NO levels were also decreased in omega-3 EFA treated group
compared to control rats (p < 0.0001). Xanthine oxidase activity was
found to be increased in omega-3 EFA treated rats when compared to the
control group (p < 0.0001). **Taken together, this preliminary animal
study provides strong support for a **therapeutic effect** of omega-3 EFA
in some neuropsychiatric disorders in which reactive oxygen species (ROS)
are recently accused to be an important physiopathogenetic factor.

PMID: 15276695 [PubMed - indexed for MEDLINE]



5: Prostaglandins Leukot Essent Fatty Acids. 2004 Sep;71(3):149-52.

Effect of fish oil supplementation on plasma oxidant/antioxidant status
in rats.

Erdogan H, Fadillioglu E, Ozgocmen S, Sogut S, Ozyurt B, Akyol O,
Ardicoglu O.

Department of Physiology, Faculty of Medicine, Gaziosmanpasa University,
Tokat 60100, Turkey. herdogan@gop.edu.tr

The aim of this study was to investigate effect of dietary omega-3 fatty
acid supplementation on the indices of in vivo lipid peroxidation and
oxidant/antioxidant status of plasma in rats. The plasma thiobarbituric
acid reactive substances (TBARS) and nitric oxide (NO) levels, and
activities of xanthine oxidase (XO), superoxide dismutase (SOD) and
glutathione peroxidase (GSH-PX) were studied in male Wistar Albino rats
after ingestion of 0.4 g/kg fish oil (rich in omega-3 fatty acids,
eicosapentaenoic acid and docosahexaenoic acid) for 30 days and compared
to untreated control rats. The rats in the treated group had
significantly higher SOD activity (P < 0.001), NO levels (P < 0.01) and
decreased TBARS levels (P < 0.05) with respect to controls whereas GSH-Px
and XO activities were not significantly different between the groups.
None of the measured parameters had significant correlation with each
other in both groups. ***We conclude that dietary supplementation of
omega-3 fatty acids may enhance resistance to free radical attack and
reduce lipid peroxidation.*** These results support the notion that
omega-3 fatty acids may be effective dietary supplements in the
management of various diseases in which oxidant/antioxidant defence
mechanisms are decelerated.  [You still reading, Monty? Is it penetrating
your DHA deficient brain??]

PMID: 15253883 [PubMed - indexed for MEDLINE]



6: Metabolism. 2004 Jan;53(1):59-65.

Effects of different dietary oils on inflammatory mediator generation and
fatty acid composition in rat neutrophils.

de La Puerta Vazquez R, Martinez-Dominguez E, Sanchez Perona J,
Ruiz-Gutierrez V.

Departamento de Farmacologia, Facultad de Farmacia, Universidad de
Sevilla, Seville, Spain.

Virgin olive oil (VOO) compared with fish oil (FO) and evening primrose
oil (PO) on the ability of stimulated leukocytes to produce inflammatory
mediators was investigated in rats. Weaned Wistar rats were fed a basal
diet (BD) (2% by weight of corn oil) or diets containing 15% by weight of
VOO, PO, or FO. After 8 weeks, glycogen-elicited peritoneal
polymorphonuclear leukocytes, mainly neutrophils, were isolated. The
calcium-ionophore stimulated neutrophils (2.5 x 10(6) cells/mL) obtained
from rats fed the different oils produced a higher release of lysosomal
enzymes (beta-glucuronidase, lysozyme, and myeloperoxidase [MPO])
compared with those fed BD. The production of reactive oxygen species
(ROS) in response to the stimulant, 12-O-tetradecanoyl-phorbol-13-acetate
(TPA), by neutrophils from the VOO group (15.44 nmol of O(2)(-) and 6.56
nmol of H(2)O(2)) was similar to the BD group (12.01 nmol O(2)(-) and
8.49 nmol H(2)O(2)) and significantly lower than the PO (20.90 nmol
O(2)(-) and 10.84 nmol H(2)O(2)) and FO (20.93 nmol O(2)(-) and 12.79
nmol H(2)O(2)) groups.  The cyclooxygenase-derived eicosanoid production
was reduced by the lipid enrichment of the diets. Whereas the generation
of prostaglandin E(2) (PGE(2)) was significantly decreased in VOO (5.40
ng/mL), PO (4.95 ng/mL), and FO (1.44 ng/mL) groups compared with BD
(8.19 ng/mL), thromboxane B(2) (TXB(2)) reduction was especially
significant in neutrophils from the FO diet group (14.67 ng/mL compared
with 26.69 ng/mL from BD). **These experimental data suggest that FO
[FISH OIL] and PO, as well as VOO, could be considered a valuable
strategy in **preventing the generation of some inflammatory mediators.**

PMID: 14681843 [PubMed - indexed for MEDLINE]



7: J Am Coll Nutr. 2003 Oct;22(5):388-99.

Effect of dietary n-3 and n-6 oils with and without food restriction on
activity of antioxidant enzymes and lipid peroxidation in livers of
cyclophosphamide treated autoimmune-prone NZB/W female mice.

Bhattacharya A, Lawrence RA, Krishnan A, Zaman K, Sun D, Fernandes G.

Department of Medicine, University of Texas Health Science Center, San
Antonio, Texas 78229-3900, USA.

OBJECTIVE: Cyclophosphamide (CTX), an alkylating agent, is extensively
used in the treatment of lupus nephritis, but its administration has been
associated with free radical mediated oxidative stress. The present study
was designed to investigate the effect of dietary corn oil (CO), fish oil
(FO) and food restriction (FR) on the activities of hepatic antioxidant
enzymes, fatty acid composition and lipid peroxidation following CTX
administration in autoimmune-prone NZB/W female mice. METHODS:
Autoimmune-prone NZB/W female mice were fed either ad libitum (AL) or
food restricted (60% of AL intake), semipurified diets containing 5% CO
or 5% FO supplemented with equal levels of antioxidants and injected with
either phosphate buffered saline (PBS), or CTX (50 mg/kg body weight)
every 10 days. Proteinuria was measured biweekly. The treatment was
stopped at 10 months and diets were continued until the mice were killed
at 12 months. Fatty acid composition, activity of antioxidant enzymes and
lipid peroxidation were analyzed in liver homogenates, and anti-DNA
antibodies were analyzed in the serum. RESULTS: Mice in the FO/AL dietary
group exhibited significantly higher liver catalase (CAT), superoxide
dismutase (SOD) and glutathione peroxidase (GSH-Px) activities compared
to the CO/AL dietary group.  CTX significantly decreased SOD and GSH-Px
activity in the FO/AL group and CAT and GSH-Px in the CO/AL group. In AL
fed mice given CTX, activities of CAT, GSH-Px and GST were significantly
higher in mice fed FO diets than in mice fed CO diets. FR increased the
activity of enzymes in both the CO and FO diet groups. In FR mice, CTX
decreased CAT and GSH-Px activity in both the CO and FO dietary groups,
but glutathione S-transferase (GST) only in the CO group. The decrease in
SOD activity was not significant in either of the restricted groups.  CTX
significantly increased generation of thiobarbituric acid reactive
substances (TBARS) in both AL groups. FR significantly decreased lipid
peroxidation in both the CO and FO groups, with or without CTX. CTX
decreased serum anti-DNA antibody levels in both the CO and FO dietary
groups. FR also decreased antibody titer in both the CO and FO dietary
groups, and it was decreased further with CTX treatment. FO fed animals
had higher levels of n-3 fatty acids, whereas CO fed animals had high
levels of n-6 fatty acids.  CTX significantly increased 20:4 and
decreased 18:1 in CO/AL fed animals, whereas it increased 18:1 and
decreased 22:6 in FO/AL fed animals. CONCLUSIONS:  Results obtained in
the present study suggests that FO [FISH OIL] and, more significantly, FO
combined with FR [food restriction] can have a **beneficial effect** in
hepatic tissues subjected to CTX induced **oxidative stress by regulating
the activity of antioxidant enzymes.** In addition, the study also
indicates that n-3 and n-6 dietary lipids are susceptible to lipid
peroxidation, particularly in the presence of a prooxidant like CTX, and
that FR is beneficial in decreasing lipid peroxidation.  The study also
suggests that FO and CTX can have **additive** effects in preventing
kidney disease in NZB/W mice.

PMID: 14559931 [PubMed - indexed for MEDLINE]




8: Nutrition. 2003 Oct;19(10):837-42.

Decreased oxidative stress in patients with ulcerative colitis
supplemented with fish oil omega-3 fatty acids.

Barbosa DS, Cecchini R, El Kadri MZ, Rodriguez MA, Burini RC, Dichi I.

Laboratory of Biochemistry, Londrina State University, Londrina,
Parana, Brazil.

OBJECTIVE: The potential pathogenicity of free radicals may have a
pivotal role in ulcerative colitis. Fish oil omega-3 fatty acids exert
anti-inflammatory effects on patients with ulcerative colitis (UC), but
the precise mechanism of the action of fish oil on oxidative stress is
still controversial. The aim of the present work was to verify the blood
oxidative stress in patients with UC and determine whether the
association of sulfasalazine to fish oil omega-3 fatty acids is more
effective than isolated use of sulfasalazine to reduce the oxidative
stress. METHODS: Nine patients (seven female and two male; mean age = 40
+/- 11 y) with mild or moderate active UC were studied in a randomized
crossover design. In addition to their usual medication (2 g/d of
sulfasalazine), they received fish oil omega-3 fatty acids (4.5 g/d) or
placebo for 2-mo treatment periods that were separated by 2 mo, when they
only received sulfasalazine. Nine healthy individuals served as control
subjects to study the oxidative stress status. Disease activity was
assessed by laboratory indicators (C-reactive protein, alpha1-acid
glycoprotein, alpha1-antitrypsin, erythrocyte sedimentation rate,
albumin, hemoglobin, and platelet count), sigmoidoscopy, and histology
scores. Analysis of oxidative stress was assessed by plasma
chemiluminescence and erythrocyte lipid peroxidation, both induced by
tert butyl hydroperoxide (t-BuOOH) and by plasma malondialdehyde.
Antioxidant status was assayed by total plasma antioxidant capacity
(TRAP) and microsomal lipid peroxidation inhibition (LPI). Superoxide
dismutase (SOD) and catalase erythrocyte enzymatic activities were also
determined. RESULTS: No significant changes were observed in any
laboratory indicator or in the sigmoidoscopy or histology scores, with
the exception of erythrocyte sedimentation rate, which decreased with
both treatments. Oxidative stress was demonstrated by significant
decreases in TRAP and LPI levels, increased chemiluminescence induced by
t-BuOOH, and higher SOD activity in patients with UC. Treatment with fish
oil omega-3 fatty acids reverted the chemiluminescence induced by t-BuOOH
and LPI to baseline levels but that did not occur when patients received
only sulfasalazine. Levels of plasma malondialdehyde, erythrocyte lipid
peroxidation, and catalase were not different from those in the control
group.  CONCLUSIONS:  **The results indicated that plasma oxidative
stress occurs in patients with UC, and there was a significant decrease
when the patients used sulfasalazine plus fish oil omega-3 fatty acids.**
However, there was no improvement in most laboratory indicators,
sigmoidoscopy, and histology scores. **The results suggested that omega-3
fatty acids may act as free radical scavengers protecting the patients
against the overall effect of oxidative stress.*** READ IT AGAIN, MONTY

Publication Types:
    Clinical Trial
    Randomized Controlled Trial

PMID: 14559317 [PubMed - indexed for MEDLINE]



SBH

From: sbharris@ix.netcom.com
Newsgroups: soc.senior.health+fitness,misc.health.alternative,sci.med.nutrition
Subject: Re: Scientists discover how fish oil protects the brain
Date: 12 Sep 2005 18:32:15 -0700
Message-ID: <1126575135.778307.66620@g44g2000cwa.googlegroups.com>

montygram wrote:
> How do they know that DHA is concentrated in everyone's brain?  My
> relatives who have lived longer than all the others never ate fish or
> used canola or flax oil, yet lived to be 100 or nearly 100.  None had
> any dementia problems.  If DHA is concentrated (please provide a
> citation to an on point study) in the brain, it must stay there
> throughout one's life.

COMMENT:
No, Monty, the turnover of PUFAs in brains occurs with half-lives of 1
to 2 weeks. And it doesn't matter if your relatives ate no canola or
flax and never ate fish. Arachadonate is made (unless you're a cat)
from linoleic acid, present in all plants. And DHA is made from alpha
linolenate, which is present to a minor degree in most plant oils
(though some are better than others). I suppose your grandparents never
ate a walnut either?  How the hell do you know what they ate?

Anyway, here's your abstract:


Curr Opin Clin Nutr Metab Care. 2002 Mar;5(2):133-8.
Long-chain polyunsaturated fatty acid accretion in brain.

Qi K, Hall M, Deckelbaum RJ.

Institute of Human Nutrition and Department of Pediatrics, Columbia
University, New York, New York 10032, USA.

Brain is highly enriched in long-chain polyunsaturated fatty acids (PUFAs),
particularly arachidonic acid and docosahexaenoic acid, which play
important roles in brain structural and biologic functions. Plasma
transport, in the form of free fatty acids or esterified FAs in
lysophosphatidylcholine and lipoproteins, and de-novo synthesis
contribute to brain accretion of long-chain PUFAs. Transport of
long-chain PUFAs from plasma may play important roles because of the
limited ability of brain to synthesize long-chain PUFAs, in the face of
high demand for them. Although several proteins involved in facilitated
fatty acid transport (e.g. fatty acid transport protein, fatty acid
binding protein and very-long-chain acyl-coenzyme A synthetase) have
been found in brain, their roles in fatty acid accumulation in brain
are poorly defined. The primary pathways that are involved in
long-chain PUFA accumulation in brain may vary according to brain
region and developmental stage.

Publication Types:
    Review
    Review, Tutorial
PMID: 11844978 [PubMed - indexed for MEDLINE]


You asked for the reference. Read it and *its* references, and learn
something.



> The most important thing here, though, are the questions about A) how
> they know that everyone has a great deal of DHA in their brains, and B)
> how can it be explained that those who seem to be healthiest and live
> longest stay away from fish, flax, and canola.

They know because it's been measured in adult brains. DHA is the most
common of the fatty acids in brains.

The healthiest populations in the world are fish-eaters. This has been
pointed out to you half a dozen times, and your own answer is to
counter with the anecdotal examples of your own ancestors. Well, sorry,
but it doesn't balances. We don't even know your name, and we sure as
hell don't know you ancestors. And when it comes to comparing thier
demographics do those of millions of Japanese (especially Okinawnans),
Icelanders, and the like, you're going to get nowhere with the
grandparent stories. So how about just laying off it?


> Without the arachidonic acid in your cells, you don't need fish oil at
> all, because it's only "benefit" is to interfere with arachidonic acid
> metabolization,


COMMENT:

Arachadonate is essential for life. If you're not fed it, you will make
it. From plant oils like triglycerides containing linoleic acid (corn
oil, etc).  Read a book.

Better yet, have your own personal blood fatty acid profile analyzed by
someplace like Efalab:

http://www.essentialfats.com/labspace.htm

Any lab will draw your blood and send it, so long as you're willing to
pay for it. You'll find plenty of arachadonate and long chain w-3's in
your own blood, I promise. Maybe not as many as if you ate right, but
enough to show you that you can't get rid of them, and your body makes
them out of the (few) w-6 and w-3 sources you do eat.

And it's all cheaper than those dumb and long animal tests you want to
do. And it might teach you almost as much.

Of course, I doubt you'll do it.

SBH

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition,sci.med,misc.health.alternative
Subject: Re: Deficiency in omega-3 fatty acids tied to ADHD
Date: 12 Sep 2005 22:02:38 -0700
Message-ID: <1126584298.657257.188830@f14g2000cwb.googlegroups.com>

jaym1212 wrote:
> > .. post a reference for your "benefits of mead acid" studies.
>
> ..Thus, dietary Eicosatrienoic Acid (Mead) from a biological source can
> accumulate in leucocytes and suppress inflammatory eicosanoid
> synthesis...
>
> PMID: 8648425

COMMENT:

Interesting. Here's the whole abstract. Note the standard reminder that
you do not see mead acid in normal animals except in EFA deficiency.

J Nutr. 1996 Jun;126(6):1534-40.

Dietary (n-9) eicosatrienoic acid from a cultured fungus inhibits
leukotriene B4 synthesis in rats and the effect is modified by dietary
linoleic acid.

Cleland LG, Gibson RA, Neumann MA, Hamazaki T, Akimoto K, James MJ.
Rheumatology Unit, Royal Adelaide Hospital, Adelaide, SA, Australia.

Eicosatrienoic acid (ETrA) is the (n-9) homologue of (n-6) arachidonic
acid (AA) and (n-3) eicosapentaenoic acid (EPA). ETrA can be
synthesized endogeneously, but tissue levels are normally undetectable
except in essential fatty acid (EFA) deficiency. An ETrA-rich oil
extracted from a cultured fungus was used to prepare diets which had
varying levels of ETrA (0-8 g/kg diet) in combination with one of two
levels of linoleic acid (LA, 2.2 or 9.5 g/kg diet). All diets were
sufficient in essential fatty acids. Groups of rats were fed these
diets for 4 wk after which leucocyte fatty acid content and leukotriene
B4 (LTB4) synthesis were measured. The influence of dietary LA on ETrA
accumulation in cells was studied and correlations with LTB4 synthesis
determined. ETrA was
efficiently incorporated into peritoneal exudate cell (PEC)
phospholipids with no evident saturation being observed with levels up
to 10 mol/100 mol total fatty acids in peritoneal exudate cells.
Cellular ETrA levels were lower (P < 0.001) in rats fed the higher
level of LA. ETrA accumulation in peritoneal exudate cells correlated
(r(2) = 0.63, P < 0.05) with reduced LTB4 synthesis which was
attributable to LTA hydrolase inhibition. Thus, dietary ETrA from a
biological source can accumulate in leucocytes and suppress
inflammatory eicosanoid synthesis. The findings justify further studies
into the biochemical and anti-inflammatory effects of dietary ETrA,
which could be incorporated into palatable food additives.

PMID: 8648425 [PubMed - indexed for MEDLINE]


A further note is that nature didn't not give you an inflammatory
response for no reason but to make you sick and old. It's an essential
component of healing and infection fighting.  Mead acid from dietary
sources may modify it, may decrease it, but that's not necessarily good
or bad. My own guess is that it depends. Are the antiinflammatory
corticosteroids good or bad for you?  That depends also.

SBH

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: soc.senior.health+fitness,misc.health.alternative,sci.med.nutrition
Subject: Re: Scientists discover how fish oil protects the brain
Date: 16 Sep 2005 13:25:28 -0700
Message-ID: <1126902328.439499.237230@g43g2000cwa.googlegroups.com>

montygram wrote:

> And how in the world do those studies SBHarris cites in any way
> demonstrate that omega 3s and 6s are essential?

Because, as I said, you cannot grow cells in culture without w-3 or w-6
PUFAs.  If you do, they fill up with mead acid (w-9), which they are
perfectly capable of making for themselves and then they DIE. You can
save them by adding a little w-3 and w-6 back into culture, but if you
don't, they're doomed. Much the same happens with rodents. I don't know
if anybody has had the time or patients to carry out such feeding
deficiency experiences in any other species to the point to death, but
all the signs in dog and humans and monkeys, suggest that they too
would all suffer chronic disese and die on a diet completely free of
w-3 and w-6 (which coconut oil is not, of course).

In any case, the mead acid does not save them with cells or mammals
from EFA PUFA deficiency. W-6 and w-3 fatty are fatty acids that act
exactly like vitamins.

SBH

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition
Subject: Re: Enig vs. Peat - "EFAs" vs. Mead Acid: The Debate.
Date: 21 Sep 2005 17:39:53 -0700
Message-ID: <1127349593.824069.246630@g44g2000cwa.googlegroups.com>

montygram wrote:
> "A Reply to Ray Peat
> on Essential Fatty Acid Deficiency"
>
> By Mary G. Enig, PhD
>
> Ray Peat, PhD, is an influential health writer who
> claims that there is no such thing as essential fatty
> acid (EFA) deficiency. According to Peat, the body can
> make its own EFAs; furthermore, he claims that EFAs in
> the body become rancid and therefore cause cancer.
>
> Unfortunately, Peat does not understand the use of EFA
> by the human body. He is trained in hormone therapy
> and his training in fats and oils has been limited to
> misinformation as far as the polyunsaturated fats and
> oils are concerned.
>
> Research on EFAs is voluminous and consistent: EFAs
> are types of fatty acids that the body cannot make,
> but must obtain from food. We do not make them because
> they exist in virtually all foods, and the body needs
> them only in small amounts. The body does make
> saturated and monounsaturated fatty acids because it
> needs these in large amounts and cannot count on
> getting all it needs from food.
>
> [then where are all the dead people who didn't consume
> omega 3s in decades, such as my relatives who lived to be 100, or are
> still alive and in their 90s?  Also, the body does make a PUFA, the
> Mead acid.  And why can't she cite one on point experiment that is
> not terribly flawed?]


COMMENT:

What part of "they exist in virtually all foods" was it that you didn't
understand, Monty?

Who are these people who you think supposedly didn't consume omega-3
EFAs in "decades," ---- and how did they manage THAT? They would need
to subsist entirely on coconut oil as their ONLY fat to do this, to
have a prayer of going about it with any kind of natural diet (since
coconut oil is the only oil I can find which has w-3 levels too low to
measure), and I can't imagine how these people you're talking about,
would even begin to make up a diet where the ONLY fat is coconut oil.

What would the rest of their diet be like? It would have to be
semi-synthetic, consisting of vitamins, minerals, cellulose, separated
protein like casein (and de-fatted protein as well), and be free of all
plant matter. Are we to assume that's how YOU'VE been living? Eating
that kind of diet?  If not, you've been getting w-3 with the rest of
your plant oils.

Even palm oil has a trace of w-3 in it, so I'm not beting than coconut
has absolutely none. And coconut is 2% w-6, which is probably enough to
keep you from w-6 deficiency right there.

In any case, unless your ancestors lived on semi-synthetic diets in
which ALL fat had been relentlessly replaced by coconut oil, I don't
think we safetly conclude they should have suffered from classical EFA
w-3 deficiency. And as I said before, if your grandma was sneaking
walnuts occasionally, all bets are off.

SBH

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition
Subject: Re: Enig vs. Peat - "EFAs" vs. Mead Acid: The Debate.
Date: 23 Sep 2005 22:58:49 -0700
Message-ID: <1127541529.514919.31580@g44g2000cwa.googlegroups.com>

montygram wrote:
> Scientists have induced EFA deficiency in animals by
> feeding them fully hydrogenated coconut oil as their
> only fat. (Full hydrogenation gets rid of all the
> EFAs; coconut oil is used because it is the only fat
> that can be fully hydrogenated and still be soft
> enough to eat.) The animals developed dry coats and
> skin and slowly declined in health, dying prematurely.
> (Interestingly, representatives of the vegetable oil
> industry blame the health problems on coconut oil, not
> on fatty acid deficiency!)
>
> [A citation here is crucial, but this claim about coconut oil makes no
> sense and is misleading.  Fresh coconut oil is natural, hydrogenated
> coconut oil introduces complicating factors that a scientist tries to
> eliminate from experiments, such as toxic nickel from the hydrogenation
> process.  Since fresh coconut oils contains no omega 3s, there is no
> reason to use the unnatural hydrogenated stuff, which may indeed act as
> a strong inhibitor of what is truly needed in pregnant animals, that
> is, biochemical activity.



COMMENT:

Hydrogenated coconut oil is used in order to induce w-6 and w-3
deficiency at the same time. Something that shouldn't bother you, since
you think neither of them is essential for adult animals.

But in the dog experiment already cited, the very unusual
atherosclerotic processes induced in the EFA deficient animals were
prevented by feeding them just a little PUFA containing vegetable oil
ADDED to their hydrogenated coconut oil atherogenic diet. That pretty
much destroys all hypothesizing about nickel or some toxin in
hydrogenated coconut oil. You don't get rid of all effects of a toxin
by adding a little EFA. You can only demonstrate *deficiency* of some
vital nutrient by showing that the effects go away by simple *addition*
of the vital ingredient to the diet.

Unless you'd like to argue that there's some undiscovered chemical in
small amounts of PUFA vegetable oil that is essential to dogs, but IS
NOT essential fatty acid(s)?  This really would be rich.

SBH

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition
Subject: Re: Enig vs. Peat - "EFAs" vs. Mead Acid: The Debate.
Date: 25 Sep 2005 01:14:52 -0700
Message-ID: <1127636092.053745.222560@o13g2000cwo.googlegroups.com>

George Cherry wrote:
> Steve Harris <sbharris@ix.netcom.com> wrote in message
> news:1127541529.514919.31580@g44g2000cwa.googlegroups.com...
> >
> > montygram wrote:
> >> Scientists have induced EFA deficiency in animals by
> >> feeding them fully hydrogenated coconut oil as their
> >> only fat. (Full hydrogenation gets rid of all the
> >> EFAs; coconut oil is used because it is the only fat
> >> that can be fully hydrogenated and still be soft
> >> enough to eat.) The animals developed dry coats and
> >> skin and slowly declined in health, dying prematurely.
> >> (Interestingly, representatives of the vegetable oil
> >> industry blame the health problems on coconut oil, not
> >> on fatty acid deficiency!)
> >>
> >> [A citation here is crucial, but this claim about coconut oil makes no
> >> sense and is misleading.  Fresh coconut oil is natural, hydrogenated
> >> coconut oil introduces complicating factors that a scientist tries to
> >> eliminate from experiments, such as toxic nickel from the hydrogenation
> >> process.  Since fresh coconut oils contains no omega 3s, there is no
> >> reason to use the unnatural hydrogenated stuff, which may indeed act as
> >> a strong inhibitor of what is truly needed in pregnant animals, that
> >> is, biochemical activity.
> >
> >
> >
> > COMMENT:
> >
> > Hydrogenated coconut oil is used in order to induce w-6 and w-3
> > deficiency at the same time. Something that shouldn't bother you, since
> > you think neither of them is essential for adult animals.
> >
> > But in the dog experiment already cited, the very unusual
> > atherosclerotic processes induced in the EFA deficient animals were
> > prevented by feeding them just a little PUFA containing vegetable oil
> > ADDED to their hydrogenated coconut oil atherogenic diet. That pretty
> > much destroys all hypothesizing about nickel or some toxin in
> > hydrogenated coconut oil. You don't get rid of all effects of a toxin
> > by adding a little EFA. You can only demonstrate *deficiency* of some
> > vital nutrient by showing that the effects go away by simple *addition*
> > of the vital ingredient to the diet.
> >
> > Unless you'd like to argue that there's some undiscovered chemical in
> > small amounts of PUFA vegetable oil that is essential to dogs, but IS
> > NOT essential fatty acid(s)?  This really would be rich.
>
> Dammit, how many answers do you have to give
> to get this guy over his delusions about EFAs?
>
> George


COMMENT:

Apparently there are no limits. He has what is known in the trades as
an idee fixe or a fixed delusion, and there's no arguing with it. He
thinks his grandparents never got any w-3, even though we know what's
essentially impossible unless they were on hyper-al, and he thinks the
various animal experiments which produced EFA deficiency in animals and
cells are due to some wierd toxicity of hydrogenated coconut oil, even
though the weird toxicity is ameliorated as completely as symptoms of
scury, when you add a teaspoon of lime juice a day. Which should tell
even the doltest of dolts that there's something essential in the lime
juice. And in this case, since our lime juice is PUFA containing plant
oils, draw your own conflusions. They work on cells in dishes, too,
dying not because their fats are hydrogenated coconut oil, but because
they've been given no fat at all. They make mead acid, but it doesn't
save them. PUFAs do. Monty ignores this.

Monty can't think, is the problem. He is unable to inductively reason
about this subject. Playfully, I hypothesize that it's because his
brain is apparently a bit short of needed best amounts of EFAs, so it
doesn't work optimally. It's a sort of chicken and egg problem, really,
to get him to realize the problem. He can't get his brain to work till
he takes EFAs, and until his brain works, he won't take EFAs. I think
if somebody just spiked his diet with Canola for a month, he'd be a new
man. Certainly a less mechanical one. At the moment I'm beginning to
wonder if EFA deficient people really pass the Turing test.

SBH

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition
Subject: Re: The Circular Logic of the "Essential Fatty Acid" Claim.
Date: 27 Sep 2005 18:26:11 -0700
Message-ID: <1127870771.513376.235570@o13g2000cwo.googlegroups.com>

montygram wrote:
> How do you know the brain is 30% plus DHA.  Where is the orginal, on
> point experiment that demonstrates this?

COMMENT:

It varies from species to species. In rodents it's actually about 70% DHA.
Here's a fascinating paper in which rats were fed artificial milk plus
linoleic acid 18:3n-6 to prevent w-6 deficiency, and some also given
either good 22:6w-3 DHA (the w-3 needed by the brain) or else the
closest artificial replacement the scientists would think of, which in
this case was DPA, which is 22:5w-6 instead of 22:6n-3 (ie, DHA with
the last n-3 bond reduced, so it's w-6, ie, "DPA").

These rats were n-3 deficient, but were getting artificial DPA, a 22
carbon PUFA even better than mead acid, since it was w-6 not w-9. Which
they tried to use in place of DHA in their brains. They still came out
worse on spacial tests, as did the animals that got only the w-6 LA (so
DPA was not itself toxic). But it's amazing how well they did. You
apparently don't die if you're w-3 deficient (unlike the case with
w-6), but you do get dumber at spacial problems. No fish, no Einstein.


J Neurochem. 2005 Aug 31; [Epub ahead of print]

An extraordinary degree of structural specificity is required in neural
phospholipids for optimal brain function: n-6 docosapentaenoic acid
substitution for docosahexaenoic acid leads to a loss in spatial task
performance.

Lim SY, Hoshiba J, Salem N Jr.

Division of Marine Environment and Bioscience, Korea Maritime
University, Busan, Korea.

Abstract This study was conducted to determine whether provision of
preformed dietary docosapentaenoic acid (DPAn-6) can replace
docosahexaenoic acid (DHA) for brain function as assessed by spatial
task performance. A newly modified artificial rearing method was
employed to generate n-3 fatty acid-deficient rats. Newborn pups were
separated from their mothers at 2 days of age and given artificial rat
milk containing linoleic acid (LA), or LA supplemented with 1% DHA
(DHA), 1% DPAn-6 (DPA) or 1% DHA plus 0.4% DPAn-6 (DHA/DPA). The
animals were then weaned onto similar pelleted diets. At adulthood,
behavioural tasks were administered and then the brains were collected
for fatty acid analysis. The LA and DPA groups showed a lower (63-65%)
brain DHA than the dam-reared, DHA
and DHA/DPA groups and this loss was largely compensated for by an
increase in brain DPAn-6. The brain fatty acid composition in the DPA
group was the same as that in the LA group at adulthood. In the Morris
water maze, the LA and DPA groups exhibited a longer escape latency
than the dam-reared and DHA groups and had a defect in spatial
retention. In conclusion, DPAn-6 could not replace DHA for brain
function, indicating a highly specific structural requirement for DHA.

PMID: 16135079 [PubMed - as supplied by publisher]

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition
Subject: Re: What does the latest "study" really tell us about eating fish?
Date: 12 Oct 2005 19:16:41 -0700
Message-ID: <1129169801.648370.81820@z14g2000cwz.googlegroups.com>

montygram wrote:
> I read a report of this study in Newsday newspaper, page A5, 10/11/2005
> - that is the source of my information.  Let's review it:
>
> 1.	It is from the good people at Rush, who would not even answer a
> basic question I put to them about a previous "study" of theirs
> that concluded that "saturated fat," but not "animal fat" was
> "associated" with Alzheimer's disease (AD) among a group of
> people who did not consume any appreciable amount of coconut oil or
> palm kernel oil.  How is this possible?  They would not answer when I
> asked.  After thinking it over, I realized what they had done, which
> was to note that items like pork and beef were less healthy than
> chicken and fish (in general).  Why didn't they just say that, as
> other researchers have?  I don't know, but I doubt you will get an
> answer if you ask them.  I couldn't.


COMMENT:

They probably figured you were unable to understand a logistic
regression on variables of food composition. Yes, it's always possible
in logistic regressions to get a variable that is a proxy variable
(marker variable) for the true causal agent. In this case, it's always
possible saturated fat is a proxy for something else unhealthy. And for
that matter, it's possible that fish-eating is a proxy for some other
really healthy activity. Just unlikely.



> 2.	It appears that they are mining the same sources they did for the
> other study.  They give simple tests to old people and also ask them to
> fill out questionnaires about what they ate.  Many of them went on to
> develop AD within a few years.  Were their memories failing before
> obvious signs of AD were present, and can we trust their memories at
> that point?  Unless there is a way to control for this, it cannot be
> considered "science."


COMMENT:
It is controlled by means of the other recalled foods of the same
eating frequency. Why would the start of Alzheimer's disease cause a
person to differentially forget that they ate (say) fish once a week,
vs. porkchops once a week?  I don't know if there were controls for
poverty of recall (to correct for people who couldn't recall ANY low
frequency items) but good studies usually do this. For just the reasons
we're discussing.



> 3.	The conclusion was "eating fish at least once a week is good for
> the brain, slowing age-related mental decline."  Now I agree that
> this makes sense, if the people ate fish low in fat as a substitute for
> beef and pork (and fried chicken, as well as a few other nasty things
> they would have eaten instead).  But what about those great omega 3
> PUFAs, you ask?  On to the next item:
>
> 4.	"The researchers looked for, but failed to find, a link between
> omega-3 fatty acids and protection from brain decline."


COMMENT:

Yes, but they did find a link between long chain omega-3's and brain
decline. It's DHA that is in brains. If you dilute out that effect by
looking at ALL omega-3's in the diet (including ALA from plants which
isn't converted well to DHA) you may not find any effect. Which they
did not.



> Just as I
> have said here many times, it is not that fish is so good, but that
> beef and pork (especially they way they are processed, prepared,
> cooked, etc.) are so bad.

COMMENT
No, you're mis-reading the study.  If you improperly lump in non-fish
omega-3, you don't find brain protection. But you wouldn't expect to.
It's not the plant omega-3's the normal human brain is made of. It's
the fish omega-3's.

> I've eaten canned tuna which had a label
> that said 0 grams of fat, so the fat is not the issue.

COMMENT:
That just means they picked their serving size to get the fat below 1
gram, meaning they can legally put down "0". It doesn't mean it really
is zero. That doesn't mean tuna doesn't have a lot of w-3 per calorie.
Is has hundreds of times more than your coconut oil, and more than any
other meat you can name.


>  Basically,
> canned tuna with 0 grams of fat is a good source of protein, though a
> bit serotogenic (so eating a lot would be unhealthy, though that was
> not the case among these old folks) and the mercury levels could be a
> concern to some.  In other words, compared to a fried steak, high in
> iron, oxidized cholesterol, arachidonic acid and other PUFAs, etc.,
> something like canned tuna is much better.


COMMENT:
No. Again, it is true that fish is relatively low in fat (10% of
calories typically, and almost never more than 15%), but if you look at
it as grams w-3 per calorie, your tuna still beats your other meats by
a mile. Sorry for your hypothesis. Guess you'll have to stop eating it.

SBH

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition
Subject: Re: coconut and no milk people and infant death
Date: 19 Oct 2005 21:12:03 -0700
Message-ID: <1129781523.134031.32450@g43g2000cwa.googlegroups.com>

montygram wrote:
> If you don't understand that a long chain polyunsaturated fatty acid
> will ramp up biochemical activity on some, if not many levels (as
> opposed to a similar chain length saturated fatty acid) then you
> ignorance is such that there's no point in discussing the matter
> further.  Take an adult ed. biochemistry course and then we can
> continue.


Monty, I've had more biochem courses than you have, unless you have a
degree in it. I know so much biochem that I have some idea of how much
of it I don't know. You haven't yet gotten to that stage, apparently.


> For those who are objective:
>
> In one of the studies used by "EFA" advocates as "proof" of their
> position, pregnant cats were given a totally saturated fatty acid diet.
>  Some kitten were born fine, but most of the pregnancies were not
> successful.  If "EFAs" were truly essential, there would have been no
> successful births.


Here's an example. FYI, Monty, the body's fat is a reservoir of all the
fatty acids you've eaten, as well as those you can synthesize. A mother
cat's fat reserves will contain some EFA, and if you feed her none, her
kittens will still get some. Just not enough. Feeding her arachadonate
isn't enough, because kittens need linoleic acid also (see below).


>  However, the fact that most were not suggests
> strongly that in this context the extra biochemical activity that PUFAs
> supply would have helped.


Indeed. And you may do the same experiment with any vitamin,
particularly in animals with short gestation times in relation to the
duration the adult can survive without food. Deprive the mother during
gestation of some vitamin, and the young will suffer to a degree more
or less in keeping with how good she is at storage of essentials.  None
of this means that the vitamins are not essential, or even that they
are conditionally essential. Just that you haven't washed them
completely out, yet.


> SBHarris seems to either have extreme problems with  reading
> comprehension or is attempting some sort of shill like discrediting
> campaign.
> Let me state this clearly:  any unsaturated fatty acid can ramp up
> biochemical activity due to the instablility of the double bond (s).
> Do you not understand that in order to know whether omega 3s and/or 6s
> have some sort of magical quality that you suggest, one would have to
> compare an animal that eats omega 3s/6s and one that eats only omega 9s
> (in similar proportions)?


Monty, there is no such thing as "instability" of double bonds per se.
Double bonds occuring uncongugated with other double bonds, resist
oxidation quite well, which is why olive oil was shipped slowly over
most of the ancient world without refrigeration, more than 2 millennia
ago, without going rancid. Indeed, why it doesn't go rancid in the
olive itself, despite lack of the hard nut covering to keep out oxygen.
Double bonds in conjugation, by contrast, are more subject to free
radical attack. The more of them you have, the more susceptable they
are. But free radicals are necessary, and the body has been controlling
free radical activity from these things just fine, for as long as life
has existed.


> As I have said here over and over again, non-pregnant adult humans
> surely do not need dietary PUFAs, but pregnant women might, because
> quick growth is needed, and they may be deficient in ways not related
> to fatty acids that necessitates an added "boost"  This explain odd
> cravings that are not unusual.  Many plants use omega 6s for quick
> growth.  Otherwise, they would all be eaten and they would be extinct
> by now, due to grazing animals.


COMMENT:

Really?  I suppose there are no grazing animals on beaches where
coconuts and palm fruit germinate? You think that olives and avocados,
high in monounsaturates and which are clearly meant to be eaten by
animals, after being eaten, magically pass through the animals'
digestive tracts and then are deposited and somehow germinate in
animal-free conditions?  Doofus!

Nuts don't want to be eaten (which is why they provide no fruit) but a
nut is a nut, Monty. The only reason tropical nuts (and fruit like
olives and avocados) contain fewer double bonds is the plants that make
them and use them, don't have to stay flexible in cold climates. That's
it. It has nothing at all to do with herbivorous animals, which FYI
occur everywhere plants do.

>  Thus, an experiment must control for
> this possibility.  It would be easy to do if you feed mice fresh
> coconut oil, then feed those mice to pregnant cats.  I am willing to
> pay for this experiment, if I am wrong.


Monty, there's no reason to do this experiment with pregnant cats, for
even kittens need EFAs. And no reason to think you need to feed them to
them with fancy mice diets, for you can feed PUFA vegetable oil in
addition, and the kittens' deficiency clears up and they grow fine. End
of story. Tuna oil, however, does not replace safflower oil. A nice
controlled experiment showing that there's something in safflower oil,
but not tuna oil, that growing kittens need. I leave you to come up
with some tortured biochemical explanation other than the obvious one.

J Nutr. 1983 Jul;113(7):1422-33.

Role of linoleate as an essential fatty acid for the cat independent of
arachidonate synthesis.

MacDonald ML, Rogers QR, Morris JG.

To determine the essential fatty acid (EFA) requirements of the cat,
specific pathogen-free kittens were fed either a linoleate-deficient
diet or one of two diets containing 5% safflower seed oil (SSO) with or
without 0.2% tuna oil. The diets were fed for 82-101 weeks beginning at
3 months of age. The results showed that linoleate is an essential
fatty acid for the cat. Linoleate deficiency resulted in reduced feed
efficiency (in males), high rates of transepidermal water loss, poor
skin and coat condition, and fatty liver. These manifestations of EFA
deficiency were prevented by SSO. Tuna oil had no additional effect.
Analyses of the fatty acid composition of plasma, erythrocytes and
liver lipids revealed that linoleate deficiency caused changes that
were qualitatively, but not quantitatively similar to EFA deficiency in
the rat. When SSO was provided, linoleate was elongated and desaturated
at the delta 5 position to form 20:2n6 and 20:3(5,11,14). However,
there was negligible conversion of linoleate to arachidonate. These
results indicate that linoleate has specific functions as an EFA,
independent of arachidonate synthesis and prostaglandin formation.
PMID: 6408230 [PubMed - indexed for MEDLINE]

SBH

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition,sci.life-extension,sci.med
Subject: Re: For Montygram- endocannabiod and arachidonic acid
Date: 31 Oct 2005 13:29:37 -0800
Message-ID: <1130794177.564629.228670@z14g2000cwz.googlegroups.com>

lian wrote:
> first forget my bad english, cause it's not my language  (I am from
> Israel).
>
>
> I got convinced by the logic to avoid EFA in order to decrease
> inflammation. And I do follow it actually for the last 2 months.


COMMENT:

Don't lump all EFA into one group. There are w-6 PUFAs which are (as a
crude generalization) inflammatory (exceptions being GLA and DHGLA),
and there are the w-3 EFAs: ALA, DHA, and EPA, which are generally
anti-inflammatory.


> But I keep worry maybe I risk myself. Espcially I am concerning the
> state of my brain cause I am prone to depression. Lately I read 2 thing
> that again raised this worry.
>
> 1.  endocannabiod (anandamide) are neuroprotective. They are
> synthesized from arachidonic acid (anandamide=amide bond +arachidonic
> acid).
> They are actually 2-arachidonoyl glycerol.

COMMENT:
Actually, anandamide is arachadonylethanolamine. But 2-arachidonoyl
glycerol works the same way. This is the receptor activated by THC.

Yes, w-6 things like LA and arachidonate are pro-inflammatory. But as
you point out, both 2-arachidonoyl glycerol and anandamide are your
brain's own inner version of cannabis, and they're both based on
arachadonate. You're not going to make them without some w-6 somewhere.
And there is some mild evidence that fish oil suppresses production of
these things in the brain.  There's even a book out claiming that w-3's
are appetite suppressive. The author thinks it's because they are
anti-inflammatory, but I think it makes more sense that w-3's suppress
appetite by the anti- endocanabinoid mechanism (just as THC/pot
enhances appetite in the same fashion). Pot gives you the munchies, and
fish oil kills the munchies.  Next, we'll be hearing that fish makes
people uptight, ambitious, and obscessive. I hearby name this the
"Captain Ahab Syndrome" (maybe the Nipponese "take over the world"
syndrome...??).

Fish, the anti-pot. Maybe if Ahab had smoked a bit more rope, Moby Dick
could have lived in peace. Perhaps if the Japanese had had a bit more
ganja with all that fish, we might not have had a Pearl Harbor. I mean,
think about it.


> MY QUESTIONS TO YOU:
> A.  If I  avoid dietary arachidonic acid, will I have too little
> endocannabiods?
> B. I f I want to be "on the safe side",  should  I consume dietary
> arachidonic acid, given it will be from the best source? (most
> un-processed, stable, un-oxidated source)?
> Given that I'm not going to take any COX-2 inhibitor?


COMMENT:

The only way to get arachadonate is eat a lot of meat. And there's
nothing like a big, juicy filet mignon to give you a little "ananda."
So there might be something to it....

SBH

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition,sci.life-extension,sci.med
Subject: Re: For Montygram- endocannabiod and arachidonic acid
Date: 31 Oct 2005 19:27:39 -0800
Message-ID: <1130815659.864459.39200@g44g2000cwa.googlegroups.com>

lian wrote:
> thanks for the replies.
>
> Sbharris, you wrote "You're not going to make them without some w-6
> somewhere"
> and Monty wrote "Everything AA does the Mead acid does in a more
> attentuated, less dangerous way".
> Do you think Monty is right, so I can count on the Mead acid to create
> 2-arachidonoyl glycerol and anandamide ? I wish this is the case, but
> how can I know?


COMMENT:

Mead acid is omega-9 (20:3n-9), an elongation product of oleic acid
(18:1n9). The body is not able to make n-6 or n-3 double bonds, and so
the diet must contain these if the body is to have any mediators like
arachidonate (AA) which is n-6. These are essential for life.
Inflammation is not a bad thing, or nature wouldn't have invented it.
It is, in fact, the universal alarm signal for healing, and infection
defense, and it is involved in normal growth, development, and repair,
as well.

Humans can make arachidonate out of any n-6, so you don't have to eat
it at all (unlike the case with the cat family). However, a diet
without any n-6 will result in severe dermatitis and hairloss (very
like chemotherapy), since all mammalian cells require some n-6 acids
for life. If the skin cannot repair itself, it falls apart.

This has been explained to Monty multiple times. If you don't give
mammalians cells in culture any n-6 PUFAs, they fill up with Mead acid
(20:3n9) and THEN THEY DIE. You cannot keep mammalian cell cultures
alive without w-6. Life in mammalian cells cannot be sustained without
an outside source of n-6 EFAs. Despite what Monty says, Mead acid is
not found in appreciable amounts in the tissues of any animal eating
its normal diet. It is evidentally something mammals produce as a last
result under conditions of n-6 deficiency (for which it is used as a
marker), but it's not enough. Biochemistry and cell-culture are enough
to tell you that, but if you don't believe those, there are multiple
animal experiments showing some n-6 is strictly necessary for all
experimental animals. Monty has found something wrong with each
experiment. The rest of the scientific world ignores him.

The amount of n-6 needed in a normal diet is small, and the amount of
n-3 is even smaller (and here the effects seem limted to the brain).
It is virtually impossible to eat a diet of any whole foods which is
deficient in n-6, but that doesn't mean it's not essential. It's almost
impossible to eat a diet of whole fresh foods deficient in vitamin C
also, but that doesn't mean scurvy can't be produced by artificial
means or very restricted foods and preparations.

Monty is something like a nut who is convinced that vitamin C is
non-essential, because he subsists healthily on a diet free of oranges.
Or even a diet free of fruits and vegetables. Ignore him. A test of his
blood would show he's getting enough, but like all fanatics, he refuses
to look.

SBH

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition,sci.life-extension,sci.med
Subject: Re: For Montygram- endocannabiod and arachidonic acid
Date: 1 Nov 2005 12:46:29 -0800
Message-ID: <1130877989.913355.225550@g49g2000cwa.googlegroups.com>

Doug Freese wrote:
> > If they do
> > eat their food, you'll start to see them die much sooner than the
> > coconut oil mice, and then you will have the evidence you appear to
> > need to feel safe.
>
> Will somebody please beam him up to the land of coconut trees.
>
> -DF


COMMENT:

I think that's Oompa Loompa Land. I've been expecting the Wang Doodle
to get Monty at any time.

And for the third time, Monty, fish-eating populations live longer than
any others. And there are no coconut eating populations who don't also
eat a lot of fish (though the reverse is NOT true, and yet doesn't
affect life span). If your brain wasn't so short of w-3's, you might be
able to infer the implications of those facts.

SBH

PS. Unlikely some doctor will ever tell me I've got a month to live. I
am a doctor, so if this task becomes necessary, I'll use the mirror.