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).

Source: www.sciencedaily.com
5/25/2005 Study Links Brain Fatty Acid Levels To Depression

Bethesda, MD -- A group of researchers from Israel has
discovered that rats exhibiting the signs of depression have
increased levels of the omega-6 fatty acid, arachidonic acid,
in their brains. The details of their findings appear in the
June issue of the Journal of Lipid Research, an American
Society for Biochemistry and Molecular Biology journal.

During recent years, omega-3 fatty acids have enjoyed
increased popularity as numerous studies have shown that
supplementing diets with fish oil (a natural source of this
polyunsaturated fatty acid) does everything from reducing the
risk of heart disease to preventing arthritis. There is also
evidence that depression may be associated with a dietary
deficiency in omega-3 fatty acids. This "phospholipid
hypothesis" of depression has been supported by research
showing that omega-3 fatty acid concentration in the blood of
depressed patients is lower than that in control patients.

"The "phospholipid hypothesis" of depression postulates that
decreased omega-3 fatty acid intake, and hence, perhaps
decreased brain omega-3 fatty acid content, could be
responsible for the disease," explains Dr. Pnina Green of Tel
Aviv University. "In humans, because of high dietary
variability and the obvious inability to examine brain tissue,
the theory is backed up mainly by indirect evidence. The
availability of the Flinders Sensitive Line rat, an animal
model of depression, overcomes both these obstacles."

In the Journal of Lipid Research study, Dr. Green in
collaboration with Dr Gal Yadid of Bar-Ilan University, Ramat
Gan, used the Flinders Sensitive Line rats to investigate the
link between omega-3 fatty acids and depression. They examined
the brains of the depressed rats and compared them with brains
from normal rats. Surprisingly, they found that the main
difference between the two types of rats was in omega-6 fatty
acid levels and not omega-3 fatty acid levels. Specifically,
they discovered that brains from rats with depression had
higher concentrations of arachidonic acid, a long-chain
unsaturated metabolite of omega-6 fatty acid.

Arachidonic acid is found throughout the body and is
essential for the proper functioning of almost every body
organ, including the brain. It serves a wide variety of
purposes, from being a purely structural element in
phospholipids to being involved in signal transduction and
being a substrate for a host of derivatives involved in
second messenger function.

"The finding that in the depressive rats the omega-3 fatty
acid levels were not decreased, but arachidonic acid was
substantially increased as compared to controls is somewhat
unexpected," admits Dr. Green. "But the finding lends itself
nicely to the theory that increased omega-3 fatty acid intake
may shift the balance between the two fatty acid families in
the brain, since it has been demonstrated in animal studies
that increased omega-3 fatty acid intake may result in
decreased brain arachidonic acid."

Although far less attention has been paid to dietary
requirements for omega-6 fatty acids, which can be found in
most edible oils and meat, perhaps in the future depression
may be controlled by increasing omega-3 fatty acid intake and
decreasing omega-6 fatty acid intake.

     >>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

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
21:3n-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
22:3n-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]

Are you trying to prove my point with these "studies?" They do
exactly what I have been pointing out here for years, that is:
they mention the 1930 study, but fail to mention that not all
essential nutrients were known - thus there is no way such a
study could be anything but worthy of a follow-up, which
nobody has ever done. I have proposed such an experiment, on
dogs (a better animal model than the 1930 rat experiment), but
have had no takers to my offer (to sum it up: if the adult
animals consuming only trace amounts of omega 3 and 6 PUFAs
live at least as long as the ones consuming supposedly
adequate amounts, you pay, but if they live a statistically
significant less amount of time, then I'll pay for it - same
diet otherwise for both groups of dogs). They say they've done
an experiment on brain cells
- did they use the alternative PUFA, the omega 9 Mead acid?
No, of course not, that would mean actually doing something
scientifically valid.

And, of course, none of this means that adults need omega 3s
or 6s. They say omega 3s are needed for immune function, but
it's been demonstrated over and over again that omega 3s are
highly immunosuppressive. It's the ability to counteract the
incredibly dangerous omega 6, arachidonic acid, that is being
demonstrated in such experiments, not a "need" for them. They
fail to mention anything about people like my grandparents,
who are mid 80s - early 90s, and never had anything beyond a
few molecules of omega 3s all their lives (they don't eat
canola oil, flax, fish, DHA enhanced eggs, etc.), but are in
pretty good shape, probably because of the chocolate and
coffee they consume. They also don't talk about how Eskimos on
diets high in omega 3s died so young, usually around the age
of 40, due to the effects of these fatty acids (bleeding
strokes, death from internal bleeding due to minor traumas,
shock from minor traumas, etc.).

The bottom line: no experiment that is directly on point, even
in an animal model, has been done to demonstrate that omega 3s
and 6s, in any amount, are required for adult humans (in the
way that vitamin B12 is, for example), and there are
thousands, if not tens of thousands, of studies that
demonstrate how dangerous these highly unstable molecules are.
There is no doubt about this - it is the scientific reality.
All the studies you can cite that supposedly claim
"essentiality" do nothing of the sort, unless you are doing
something other than science, perhaps creating a religion in
which particular PUFAs are worshipped as divine in some way.

No, I stay away from omega 3s, but I am only interested in the
scientific reality, and it is clear that if you are loaded up
with arachidonic acid, and getting destroyed by AA
metabolites, then the omega 3s will knock down the
metabolization to some degree. It is a temporary fix, and I
have cited studies that point out that after a certain period
of time, the omega 3 group actually has more problems than the
control group.

As for Burr & Burr: that is what is cited in the major
nutrition textbooks, and yet even on the level of logic, it is
unjustifiable to suggest that this rat experiment done in 1930
"proves" anything. We need to do that experiment again with
proper controls. Now if you know of such an experiment, then
go ahead and cite it. Until then, all one can say as a
scientist is that there is a huge amount of evidence against
consuming more than tiny amounts of omega 3s and 6s, and no
scientific evidence suggesting that it is "essential" in a way
that non-pregnant human adults should worry about getting more
of it. Instead, at this point in time, the reasonable person
with some scientific knowledge knows that avoiding these
dangerous substances is consistent with the evidence.

montygram wrote:
  > Are you trying to prove my point with these "studies?" They
  > do exactly what I have been pointing out here for years,
  > that is: they mention the 1930 study, but fail to mention
  > that not all essential nutrients were known - thus there is
  > no way such a study could be anything but worthy of a
  > follow-up, which nobody has ever done. I have proposed such
  > an experiment, on dogs (a better animal model than the 1930
  > rat experiment), but have had no takers to my offer (to sum
  > it up: if the adult animals consuming only trace amounts of
  > omega 3 and 6 PUFAs live at least as long as the ones
  > consuming supposedly adequate amounts, you pay, but if they
  > live a statistically significant less amount of time, then
  > I'll pay for it - same diet otherwise for both groups of
  > dogs). They say they've done an experiment on brain cells
  > - did they use the alternative PUFA, the omega 9 Mead acid?
  > No, of course not, that would mean actually doing
  > something scientifically valid.
  >
  > And, of course, none of this means that adults need omega 3s
  > or 6s. They say omega 3s are needed for immune function, but
  > it's been demonstrated over and over again that omega 3s are
  > highly immunosuppressive. It's the ability to counteract the
  > incredibly dangerous omega 6, arachidonic acid, that is
  > being demonstrated in such experiments, not a "need" for
  > them. They fail to mention anything about people like my
  > grandparents, who are mid 80s - early 90s, and never had
  > anything beyond a few molecules of omega 3s all their lives

Your rigid scientific method cracks me up.

  > (they don't eat canola oil, flax, fish, DHA enhanced eggs,
  > etc.), but are in pretty good shape, probably because of the
  > chocolate and coffee they consume.

You've got to be trolling.

  > They also don't talk about how Eskimos on diets high in
  > omega 3s died so young, usually around the age of 40, due
  > to the effects of these fatty acids (bleeding strokes,
  > death from internal bleeding due to minor traumas, shock
  > from minor traumas, etc.).

Arachidonic acid deficiency, you think?

  > The bottom line: no experiment that is directly on point,
  > even in an animal model, has been done to demonstrate that
  > omega 3s and 6s, in any amount, are required for adult
  > humans (in the way that vitamin B12 is, for example),

You're obvious desperate to be the group clown. In the post BY
YOU that started this thread it has:

"Arachidonic acid is found throughout the body and is
essential for the proper functioning of almost every body
organ, including the brain. It serves a wide variety of
purposes, from being a purely structural element in
phospholipids to being involved in signal transduction and
being a substrate for a host of derivatives involved in second
messenger function."

Are we to take it you don't believe your own hype?

  > and there are thousands, if not tens of thousands, of
  > studies that demonstrate how dangerous these highly unstable
  > molecules are. There is no doubt about this - it is the
  > scientific reality. All the studies you can cite that
  > supposedly claim "essentiality" do nothing of the sort,

Ho hum. Here's outing number five for this...

"Thirty years later, Hansen et al. [140] were the first to
describe EFAD in humans. They observed unsatisfactory growth
rates and dryness of the skin in many infants on low LA
intakes. EFAD has been most extensively described in
subjects on fat-free total parenteral nutrition
(TPN)[141-147]. For example, O'Neill et al. [142] reported
on 28 patients,ranging from newborns to 66 years old, who
received fat-free TPN. LA levels fell rapidly, followed by
AA. In most of the patients the
20:3n9/20:4n6 ratio (a biochemical marker for EFAD) had
increased after a few weeks above the 0.4 criterion
[148], followed approximately one week later by
clinical signs of a scaly and thin skin, and hair
loss. In addition to these classical EFAD symptoms,
many other biological and behavioural changes have
been documented [149-151]"

Two of the refs:

Wene JD, Connor WE, DenBesten L. The development of essential
fatty acid deficiency in healthy men fed fat-free diets
intravenously and orally. J Clin Invest 1975;56:127-34

O'Neill JA, Caldwell MD, Meng HC. Essential fatty acid
deficiency in surgical patients. Ann Surg 1977;185:535-41"

As predicted you didn't respond to this one about fatty
acid deficiency in dogs that Steve Harris pointed out to
you either:

Here's the PubMed link http://www.ncbi.nlm.nih.gov/entrez/que-
ry.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=1263442

  > unless you are doing something other than science, perhaps
  > creating a religion in which particular PUFAs are worshipped
  > as divine in some way.

Like Mead Acid you mean?

MattLB