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Medical Forum / General / Alternative / September 2005

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Scientists discover how fish oil protects the brain

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Roman Bystrianyk - 12 Sep 2005 23:12 GMT
Karen Pallarito, "Scientists discover how fish oil protects the brain",
Cincinnati Enquirer, September 12, 2005,
Link:
http://news.enquirer.com/apps/pbcs.dll/article?AID=/20050912/LIFE07/509120313/10
42/LIFE


Louisiana State University scientists say they have discovered how the
fatty acids found in fish oil help protect the human brain from the
type of cognitive decline associated with Alzheimer's disease.

Their study shows that docosahexaenoic acid (DHA), an omega-3 fatty
acid found in coldwater fish such as mackerel, sardines and salmon,
reduces levels of a protein known to cause damaging plaques in the
brains of Alzheimer's patients.

What's more, the researchers discovered that a derivative of DHA, which
they dubbed "neuroprotectin D1" (NPD1), is made in the human brain.
That natural substance plays a key role, too, in protecting the brain
from cell death, the study showed.

"Now what does this tell us from the point of view of the disease? I
believe that, obviously, diet is a major issue here," said Dr. Nicolas
G. Bazan, director of the Neuroscience Center of Excellence at the
Louisiana State University Health Sciences Center in New Orleans.

"DHA is an essential building block for the structure of brain cells,"
he noted. "And now we are finding that this building block also makes a
'golden brick' (NPD1) that helps the life of the neurons to continue."

Greg M. Cole, associate director of the Alzheimer's Disease Research
Center at the University of California, Los Angeles David Geffen School
of Medicine, said the study "provides strong evidence" that NPD1 offers
"several important protective contributions."

The study was released online Sept. 8, in advance of its Oct. 1
publication in the Journal of Clinical Investigation.

Bazan, who is currently staying in Philadelphia, had been in Poland to
give the opening lecture at a meeting on neurodegenerative diseases
when Hurricane Katrina struck New Orleans. So far, he said, he has
re-established contact with about half of the roughly 115 people who
work at the LSU neuroscience center.

Due to the state of emergency in New Orleans, the center won't resume
work until perhaps late November or early December, interrupting what
Bazan calls the most exciting period in his scientific career.

Indeed, while previous studies have suggested that DHA reduces the risk
of Alzheimer's-related cognitive deficits, scientists haven't explored
how the fatty acid may work its protective magic.

Some 4.5 million Americans have Alzheimer's disease, according to the
Alzheimer's Association. If no cure is found, as many as 16 million
could have the disease by 2050, as the population ages.

Bazan and colleagues at LSU and Brigham & Women's Hospital in Boston
conducted a series of experiments. Some of the testing involved
postmortem human brain samples harvested from six patients who had
Alzheimer's disease and an equal number of age-matched "control"
samples from people who did not have the disease.

The researchers also used technology called tandem mass spectrometry to
analyze changes within brain cells.

Studies show DHA is highly concentrated in the brain and retina of the
eye. In earlier research, Bazan's team discovered that NPD1 is produced
in cells that are critical for vision. They wondered whether the brain
might do the same.

"And the human brain, sure enough, makes neuroprotectin D1," Bazan
found.

Cole, the UCLA researcher, noted: "This study also shows that both DHA
and its NPD1 product are effective in treating human brain cells and
reducing the inflammation and toxicity from a toxin called beta amyloid
that is widely believed to cause Alzheimer's."

The researchers also examined specific areas of the brains of people
with Alzheimer's, including an area critical to memory formation and
cognition. "And that area shows huge - I mean 20-, 25-fold - decreases
in neuroprotectin D1, as compared with other areas in the same human
brain," Bazan said.

Furthermore, in cell studies designed to mimic the effects of aging,
the team found that adding DHA reduced the secretion of toxic beta
amyloid proteins and, at the same time, spurred production of NPD1.

"We are concluding that neuroprotectin D1 induces a gene expression
program that is neuroprotective, meaning that it promotes survival of
brain cells," Bazan said. And that discovery, he added, could one day
lead to the development of a new treatment to slow the progression of
Alzheimer's disease.

For now, though, people should pursue a nutritional approach to warding
off Alzheimer's and diminishing the effects of the disease.

Since DHA sources are safe, cheap, available and clinically proven to
fight heart disease, the nation's number one killer, Cole said he would
advise families of Alzheimer's patients to make sure their loved ones
get the minimum recommended DHA from their diet or supplements. Experts
recommend 200 to 300 milligrams per day, a far greater amount than the
60 to 80 milligrams daily that Americans typically get in their diet,
he noted.
Matti Narkia - 12 Sep 2005 23:36 GMT
12 Sep 2005 15:12:38 -0700 in article
<1126563158.277832.292330@o13g2000cwo.googlegroups.com> "Roman Bystrianyk"
<rbystrianyk@gmail.com> wrote:

>Karen Pallarito, "Scientists discover how fish oil protects the brain",
>Cincinnati Enquirer, September 12, 2005,
[quoted text clipped - 19 lines]
>G. Bazan, director of the Neuroscience Center of Excellence at the
>Louisiana State University Health Sciences Center in New Orleans.

This seems to refer to the same study,

Lukiw WJ, Cui JG, Marcheselli VL, Bodker M, Botkjaer A, Gotlinger K, Serhan
CN, Bazan NG.
A role for docosahexaenoic acid- derived neuroprotectin D1 in neural cell
survival and Alzheimer disease.
J Clin Invest. 2005 Sep 8; [Epub ahead of print]
PMID: 16151530 [PubMed - as supplied by publisher]
<http://www.jci.org/cgi/content/abstract/JCI25420v1>
<http://www.jci.org/cgi/reprint/JCI25420v1> (full text)
<http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=16151530>
(full text)

which was already mentioned in another today's thread, "DHA is good for the
brain, helps in Alzheimer's disease". The news report is different though,
and a lot longer. Thanks.

Signature

Matti Narkia

wizzzer@hotmail.com - 13 Sep 2005 01:22 GMT
I'm prone to depression so I take about 10 fish oil pills a day. That's
1200 mg of DHA per day, which I think is what is recommended for
depression. It makes me feel good and my memory has improved too. I get
the big bottle of 250 pills from Walmart once a month. The Omega 3
fatty acids enable more serotonin to be created. If I go for a few days
without the pills, I feel depressed and exhausted.
montygram - 13 Sep 2005 01:43 GMT
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.

The mechanism, however, is something I agree totally with.  What is
happening is that arachidonic acid metabolization is being interferred
with, and that is the "benefit."  If there is not ample antioxidant
protection, however, as the guy taking 1200 mg. a day would need, you
will have to deal with necrosis somewhere in your body and your immune
system will have problems.  The most recent study on fish oil and
immunosuppression found that the EPA was the problem, so if you take
just DHA you might not have as much of a problem, but that could be
because DHA is so unstable that is just gets oxidized into
not-so-harmful substances before it could reach your bloodstream,
though it might do damage to your stomach.

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.

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, but that does not need to be happening at all, and
therefore, you don't need to worry about all the lipid peroxidation
that will take place when you ingest fish oil, canola oil, flax oil,
and the other highly unsaturated oils.
sbharris@ix.netcom.com - 13 Sep 2005 02:32 GMT
> 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 of 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
Roman Bystrianyk - 13 Sep 2005 02:01 GMT
You may wish to consider the following as well.  Good luck and have a
great day.

DHEA may ease midlife depression
http://www.healthsentinel.com/news.php?id=617&title=DHEA+may+ease+midlife+depres
sion&event=news_print_list_item


Herb 'as good as depression drug'
http://www.healthsentinel.com/news.php?id=606&title=Herb+%27as+good+as+depressio
n+drug%27&event=news_print_list_item


Exercise Can Ease Depression
http://www.healthsentinel.com/news.php?id=581&title=Exercise+Can+Ease+Depression
&event=news_print_list_item


Depression: Cure's In Your Diet?
http://www.healthsentinel.com/news.php?id=068&title=Depression%3A+Cure%27s+In+Yo
ur+Diet%3F&event=news_print_list_item

montygram - 13 Sep 2005 02:35 GMT
I researched this claim that "DHA is enriched in brain cells" and found
nothing on point.  As I've said before, the cravings many pregnant
women have is evidence that more biochemical activity is needed, so
they avoid antioxidant herbs and spices and eat things like herring in
ice cream.   When I was recovering from osteoporosis, and started to
take calcium citrate, within 2 weeks I had strange cravings and could
not eat anything spicy, even though I really enjoyed curry dishes and
the like.  After a month or so, the cravings and revulsions
disappeared.  I did not consume omega 3s and avoided any major source
of omega 6s, yet the bone growth went great and is no longer a problem.
My body did not want me to eat foods high in antioxidants, because
this would slow the regrowth of bone.  It's likely that the same thing
is going on in pregnant women and growing children.  Adults do not need
DHA, they just need to avoid omega 3s and 6s in their diets.

The specific need for DHA has not been established by controlled
experiments.  I found a site that sums up the state of the evidence
very well.  It is at
http://www.mastersofpediatrics.com/cme/cme2004/lecture21_1.asp

If you read through here, you see that it's all based on assumptions.
Tests for "visual acuity" and the like may be arachidonic acid
metabolization inhibition.  A controlled experiment would need to be
done to determine what the scientific reality is.

When I was young, in the 60s, there was no talk of "essential fatty
acids," and everybody hated the oily fish and made fun of people who
ate them.  There was no canola oil, and nobody thought flax/linseed oil
was edible.  This was also true for my relatives who lived to be 100 or
close to it.  The children my age grew up without all the talk of ADHD
and such that you hear today.  So there is a major contradiction here -
one that nobody with the power to do experiments is addressing.
Why?  Because even if you wanted to, you would not get funding.  Try to
get a grant that is about debunking a claim that everybody now takes
for granted and see how far you get.

My explanation makes the most sense, that is, DHA and EPA inhibit the
dangerous metabolization of arachidonic acid, and so appear to be
"benefical," yet what would happen if there were no omega 3 or 6 PUFAs
at all (except tiny trace amounts)?  The oils that are used today in
Western nations are highly unsaturated with omega 6 and/or omega a3s,
yet this is something new in history.  Butter, lard, and olive oil were
the fat sources used by Westerners for hundreds of years.  Only trace
amounts of omega 3s and very small amounts of omega 6s in these fat
souces.

For the true believers, I ask you to put your money where your beliefs
are and take me up on my experiment offer.  "Prove" me wrong, and I'll
pay for the whole thing.  But if you are wrong, you pay.

I am waiting...

What is required is an experiment on old people who died with and
without dementia, AD, and similar "diseases."  Brain tissue would need
to be autopsied to see what the fatty acid compositions are.  This
would not cost a huge amount of money, but it would settle the issue.
Until then, I can't see how it is possible that the "rapid turnover" of
DHA in brain cells is possible when so many relatives had no DHA
source.  It is incredible that nobody is saying, "wait a minute, this
is not physically possible - it is science fiction;"  An example of
this kind of claim, made with no citation of an on-point experiment, is
below (try not to laugh to hard while reading it, as you might lose
some DHA by making enhancing the "turnover"):

"Health Benefits of Docosahexaenoic Acid (DHA)"
by
Horrocks LA, Yeo YK
Docosa Foods Ltd, 1275 Kinnear Road,
Columbus, OH, 43212-1155, USA,
Pharmacol Res 1999 Sep; 40(3):211-225

"...The turnover of DHA in the brain is very fast, more so than is
generally realized..."
wizzzer@hotmail.com - 13 Sep 2005 05:43 GMT
>Butter, lard, and olive oil were the fat sources used by Westerners for hundreds of
>years.  Only trace amounts of omega 3s and very small amounts of omega 6s in these
>fat souces.

I don't think that's true. I read that Americans used to eat much more
wild meat a hundred years ago. Wild meat has omega 3 fatty acids,
unlike farm raised meat. I don't think it's a trace amount either. Also
wild salmon has omega 3 fatty acids and farm raised salmon doesn't. The
article I read said that depression has increased a lot while the
eating of omega 3 fatty acids has decreased. The article said omega 3
fatty acids are needed for many human physiological functions.
Matti Narkia - 13 Sep 2005 02:34 GMT
12 Sep 2005 17:22:13 -0700 in article
<1126570933.500713.37240@o13g2000cwo.googlegroups.com> wizzzer@hotmail.com
wrote:

>I'm prone to depression so I take about 10 fish oil pills a day. That's
>1200 mg of DHA per day, which I think is what is recommended for
>depression.

No. In trials both ethyl esther of eicosapentaenoic acid A.K.A. ethyl-EPA
A.K.A. E-EPA, and fish oil have been successful. There has been only one
trial with docosahexaenoic acid (DHA) and that failed:

Marangell LB, Martinez JM, Zboyan HA, Kertz B, Kim HF, Puryear LJ.
A double-blind, placebo-controlled study of the omega-3 fatty acid
docosahexaenoic acid in the treatment of major depression.
Am J Psychiatry. 2003 May;160(5):996-8.
<http://ajp.psychiatryonline.org/cgi/content/full/160/5/996>

   "CONCLUSIONS: This trial failed to show a significant effect of DHA
    monotherapy in subjects with major depression."

Therefore the active component against depresssion seems to EPA, not DHA.

A citation from the article

Scientific studies concerning omega-3
http://en.isodisnatura.com/depression_omega-3.htm

   "The studies suggest that it is EPA that promotes positive
   emotions, rather than DHA (Nemets, Stahl et al. 2002; Peet
   and Horrobin 2002). Studies using pure DHA have shown it
   has no more effect than a placebo (Marangell, Martinez et
   al. 2003). In addition, a competition mechanism means DHA
   prevents EPA being completely assimilated and used
   (Horrobin, 2002), while by contrast, the body can
   transform EPA into DHA as required."

The page

Omega-3 Fatty Acids, Linus Pauling Institute's Micronutrient
Information Center
<http://lpi.oregonstate.edu/infocenter/othernuts/omega3fa/#disease_prevention>

is a little out of date, but there is some information about doses:

   "A preliminary placebo-controlled trial that assessed the
   effects of very high doses of EPA (6.2 g/day) and DHA (3.4
   g/day) in 30 patients with bipolar disorder (formerly
   known as manic-depressive disorder) found that those
   supplemented with EPA + DHA had a significantly longer
   period of remission than those on an olive oil placebo
   over a 4-month period (103). Patients who took the EPA +
   DHA supplements also experienced less depression than
   those who took the placebo. Although major depression
   occurs in both, bipolar disorder and depression are
   considered distinct psychiatric conditions. More recently,
   a pilot study in 30 women diagnosed with borderline
   personality disorder found that the 20 women randomized to
   treatment with 1 g/day of ethyl-EPA for eight weeks
   experienced less severe depressive symptoms than the 10
   women randomized to treatment with a placebo (104). "

DOSING:
=======

__________________________________________________________________________
!                                                                         !
!    If Ethyl-EPA is taken, the best dose seems to be 1 g/d. If fish oil  !
!    is used, the daily dose should have  6.2 g of regular EPA in it or   !
!    at least 6.6 g of regular EPA+DHA, most of it DHA.                   !
!_________________________________________________________________________!

Ethyl-EPA for depression references:
------------------------------------

Murck H, Song C, Horrobin DF, Uhr M.
Ethyl-eicosapentaenoate and dexamethasone resistance in
therapy-refractory depression.
Int J Neuropsychopharmacol. 2004 Sep;7(3):341-9. Epub 2004 Mar 05.
Review.
PMID: 15003146 [PubMed - indexed for MEDLINE]
<URL:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=15003146
>

   "Preliminary evidence shows that ethyl-eicosapentaenoate (E-
   EPA) has a marked clinical effect when used as an adjunct in
   therapy-refractory depression. EPA belongs to the class of
   polyunsaturated omega-3 fatty acids. The mechanism of its
   action in depression is not fully understood. There are two
   related fields where the pathophysiology of refractory
   depression meets the effect of EPA. First, a general
   immunosuppressive effect of EPA meets a general
   immunoactivation in severe depression, especially an increase
   in CD4/CD8 ratio, neutrophilia, and an increase in interleukins
   (IL)-6 and IL-12 and of prostaglandin E2 (PGE2). Secondly, a
   resistance to dexamethasone (Dex) suppression of the HPA axis
   meets the effects of EPA on multidrug resistance reversing and
   HPA axis suppression. The effects of EPA on the immune system,
   the HPA axis, and multidrug resistance are connected through
   the action of a transport protein called p-glycoprotein (p-gp).
   Physiological and synthetic steroids such as cortisol and Dex
   are substrates of p-gp, and so Dex resistance in depression may
   be related to dysfunction of this protein. In addition,
   expression of p-gp is induced by PGE2, and EPA inhibits the
   synthesis of PGE2. The reversal of drug resistance by EPA may
   be mediated via this immunological mechanism and lead to its
   antidepressive efficacy. In addition, antidepressants such as
   amitriptyline, which have special efficacy in severe
   depression, decrease p-gp function. EPA may, furthermore,
   enhance the action of antidepressants, like many SSRIs that are
   p-gp substrates, which are actively transported out of the
   intracerebral space at the level of the blood-brain barrier."

Peet M, Horrobin DF.
A dose-ranging study of the effects of ethyl-eicosapentaenoate in
patients with ongoing depression despite apparently adequate
treatment with standard drugs.
Arch Gen Psychiatry. 2002 Oct;59(10):913-9.
PMID: 12365878 [PubMed - indexed for MEDLINE]
<http://jerrycott.com/user/Peet.EPA.Archives.2002.pdf>

   "... At least 2 known mechanisms could lead to EPA being more
   effcetive than DHA. In depression, production of prostaglandins
   from arachidonic acid by the cyclooxygenase system has
   constantly been reported to be elevated.28-32 Eicosapentaenoic
   acid but not DHA is an effective substrate for cyclooxygenase
   and can compete with arachidonic acid at this point. Also, in
   some phospholipase A2 assays, EPA, but not DHA has been
   reported to be an effective inhibitor.33 These different
   effects of EPA and DHA, which may include synergism and
   antagonism, mean that biological effects of fish oils, which
   contain boths in highly variable proportions, will be uncertain
   and difficult to predict.

   The mechanism of action of ethyl-eicosapentaenoate requires
   much further exploration. We think it unlikely that it can be
   explained by improved pharmacokinetics or pharmacodynamics of
   existing drugs. Although individual patients may benefit from
   increasing antidepressant dosages, no substantial studies of
   existing drugs have shown such large improvements in outcome
   as a consequence of increasing the dosage as the improvement
   were seen in the 1-g/d group. No differences were seen in the
   effect of ethyl-eicosapentoaenoate between the different
   classes of aintidepresssants. Limited numbers of patients not
   receiving any antidepressant who have been treated by us in
   clinical practice have shown improvements similar to thos in
   this trial. Patients with schizophrenia not receiving any drug
   therapy have responded to EPA.19,21 Therefore, althouh
   modulation of background drug pharmacokinetics cannot entirely
   be ruled out, we think it more likely that the ethyl-
   eicosapentaenoate action is on cell membranes and signal
   transduction systems.
   
   Ethyl-eicosapentaenoate has one side effct that is likely to be
   beneficial in depression. It lowers triglyceride levels,
   inhibits platelet aggregation, and inhibits cardiac
   arrhythmias.6,34,35 In 2 large trials, EPA-containing products
   (providing EPA at dosages less than 1 g/d) have shown to reduce
   mortality related to heart disease.36,37 In view of steadily
   increasing evidence of associations between various types of
   cardiovascular disease and depression, and that both disorders
   are associated with low blood EPA levels, ethyl-
   eicosapentaenoate may be of particular benefit in depressed
   patients who are also at risk for cardiovascular disease.6

Peet M, Horrobin DF.
A dose-ranging study of the effects of ethyl-eicosapentaenoate in
patients with ongoing depression despite apparently adequate
treatment with standard drugs.
Arch Gen Psychiatry. 2002 Oct;59(10):913-9.
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1
2365878&dopt=Abstract
>

Nemets B, Stahl Z, Belmaker RH.
Addition of omega-3 fatty acid to maintenance medication treatment
for recurrent unipolar depressive disorder.
Am J Psychiatry. 2002 Mar;159(3):477-9.
<http://ajp.psychiatryonline.org/cgi/content/full/159/3/477>

Fish oil for depression references:
-----------------------------------

Su KP, Huang SY, Chiu CC, Shen WW.
Omega-3 fatty acids in major depressive disorder. A preliminary
double-blind, placebo-controlled trial.
Eur Neuropsychopharmacol. 2003 Aug;13(4):267-71.
http://tinyurl.com/67mh6
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1
2888186&dopt=Abstract
>

Other related references:
-------------------------

Horrobin DF.
Phospholipid metabolism and depression: the possible roles of
phospholipase A2 and coenzyme A-independent transacylase.
Hum Psychopharmacol. 2001 Jan;16(1):45-52.
PMID: 12404597 [PubMed - as supplied by publisher]
<http://www3.interscience.wiley.com/cgi-bin/abstract/76509908/ABSTRACT>

Peet M.
Essential fatty acids: theoretical aspects and treatment
implications for schizophrenia and depression
Advan. Psychiatr. Treat., May 1, 2002; 8(3): 223 - 229.
<http://apt.rcpsych.org/cgi/content/full/8/3/223>

Stoll AL, Severus WE, Freeman MP, Rueter S, Zboyan HA, Diamond E,
Cress KK, Marangell LB.
Omega 3 fatty acids in bipolar disorder: a preliminary double-blind,
placebo-controlled trial.
Arch Gen Psychiatry. 1999 May;56(5):407-12.
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1
0232294&dopt=Abstract
>

Signature

Matti Narkia

wizzzer@hotmail.com - 13 Sep 2005 10:45 GMT
>No. In trials both ethyl esther of eicosapentaenoic acid A.K.A. ethyl-EPA
>A.K.A. E-EPA, and fish oil have been successful. There has been only one
>trial with docosahexaenoic acid (DHA) and that failed:

OK, it's been a long time since I read about EPA and DHA so maybe I got
it mixed up. Anyway, fish oil has both of them.
Matti Narkia - 13 Sep 2005 11:09 GMT
Tue, 13 Sep 2005 04:37:40 +0300 in article
<pa8ci159iecaljc8cp0acuu1m6lscfv75k@4ax.com> Matti Narkia
<mnng1@despammed.com> wrote:

>12 Sep 2005 17:22:13 -0700 in article
><1126570933.500713.37240@o13g2000cwo.googlegroups.com> wizzzer@hotmail.com
[quoted text clipped - 18 lines]
>
>Therefore the active component against depresssion seems to EPA, not DHA.

[snip]

>DOSING:
>=======
[quoted text clipped - 5 lines]
>!    at least 6.6 g of regular EPA+DHA, most of it DHA.                   !
>!_________________________________________________________________________!

Oops, the last word should of course be EPA, not DHA:

DOSING:
=======
_________________________________________________________________________
!                                                                         !
!    If Ethyl-EPA is taken, the best dose seems to be 1 g/d. If fish oil  !
!    is used, the daily dose should have  6.2 g of regular EPA in it or   !
!    at least 6.6 g of regular EPA+DHA, most of it EPA.                   !
!_________________________________________________________________________!

Signature

Matti Narkia

Matti Narkia - 13 Sep 2005 15:02 GMT
Tue, 13 Sep 2005 13:12:43 +0300 in article
<ib9di1lkinck4f614n2lcd0cdlu3ekqpvb@4ax.com> Matti Narkia
<mnng1@despammed.com> wrote:

>DOSING:
>=======
[quoted text clipped - 4 lines]
>!    at least 6.6 g of regular EPA+DHA, most of it EPA.                   !
>!_________________________________________________________________________!

Let's make this a little simpler. For depression take either

1) 1 g Ethyl-EPA daily

or

2) Fish oil giving at least 6.2 g regular EPA daily.

If you can find Ethyl-EPA, 1) is easier to follow. If you use regular fish
oil, you have to read from the label how much EPA it has per capsule or ml,
and then calculate how many capsules or ml you have to take daily to get 6.2
of EPA. That will be quite a lot of fish oil, so it will be more difficult
to take than 1).

Signature

Matti Narkia

montygram - 13 Sep 2005 22:29 GMT
Matti is probably correct here.  Within a few years of taking such
large amounts of fish oil, you will no longer be depressed, but instead
you will be fighting for your life.

Seriously, think about what is being said:  your brain is loaded with
DHA, and the DHA is "turning over" very quickly.  Everyone agrees that
you need plenty of EPA and DHA in the diet, or possibly huge amounts of
flax oil (there is debate on this point) in order to get enough.  Very
few people I know are eating enough omega 3s to fulfill this criteria.
And there are my old relatives who laugh at the idea of eating oily
fish or flax or canola oil.  Let's not forget me, Ray Peat, and a few
othes who are making sure we get practically no omega 3s (and very
little omega 6s).  How is this "rapid turnover" occuring?  Hopefully,
some of you will realize that this claim in particular is physically
impossible.  It violates basic laws of nature.  There are not enough
omega 3 PUFAs in my diet, nor in the diets of many people I know, for
such a "rapid turnover" to take place.

Nor have any experiments been done, for example, the one I describe on
old peoples' brains, that demonstrate this claim.  It is a claim only.
It doesn't make sense scientifically.  It only makes sense in the
context of what nutrition textbooks say.  And if you read such
textbooks closely, you will see they say things like "it may" or "it
seems likely."  In other words, they don't know, but they need to put
something in the textbook or else there would be a thin pamphlet rather
than a brick-sized book, and the teacher's wouldn't know what to teach.
It is about creating the illusion of a body of knowledge in order to
justify the existence of the "discipline," and not about the scientific
method.  Then, the snake oil salesmen come along and take advantage of
the situation, telling people they need "supplements" that their
ancestors did not need to live to be 100 or whatever.

So, what is happening?  Think it terms of an overall framework.  If
you've done as much research as I have, you see that many "chronic"
conditions involve what is described as a "fatty acid deficiency" of
one or another kind of fatty acid.  All they are seeing is arachidonic
acid metablization.  When cells are physically or chemically stressed,
the AA is released, gets changed (metabolized) into dangerous molecules
like PGE2 or LTB4, and damge is done to your body.  But the AA is gone,
so you appear to be "essential fatty acid deficient" or whatever they
call it.  So they load you up with AA, and your body just changes it
over to the very dangerous metabolites.  The end results is that you
will get sicker or die sooner.  They are fixated on what is called
epiphenomena, things that are not the problem, but signs of the
problem.  Because DHA is so unstable, when you are undergoing more
oxidative stress than most people, the DHA will be changed into some
other molecule, so when blood is tested, they will say you are "low" in
DHA.  Taking DHA or EPA/DHA supplements can act to interfere with AA -
everyone agrees on that, but instead of spending billions of dollars on
moronic studies or to design drugs that many people can't even afford
(and may turn out to be another killer drug), why not get 50 dogs and
see if they live well and long without omega 3s and 6s?  If they do -
and I'm willing to put my own money up because after reading the
relevant literature I have no doubt - then all this stuff about buying
fish oil pills and so forth can be tossed aside.  As far as I'm
concerned, it is highly unethical to suggest that people ingest a
highly unstable substance when the relevant experiments (which are
cheap and easy to do) have not been done, and when there is no reason
to believe that making a body more biochemically unstabe is a good
idea.  I don't know how such people can look at themselves in the
mirror, but I would not be able to.  However, I am giving them the
opportunity to "prove" me wrong, and yet they won't even address my
proposal.  Something is very wrong with what they are telling you, but
if you want to blindly follow their advice, in light of everything I
have explained in detail here, then why even read the posts here?  Just
go to your local vitamin store and tell them to give you what's "hot"
these days.

What can be done for those without a strong scientific backgroundd?
Get to the root cause, which is usually oxidative stress.  Make your
body as biochemically stable as is possible.  You can eat berries, dark
chocolate, etc., but it's more important to avoid the highly
unsaturated oils and only eat food with cholesterol in it if it is
boiled (except for whole milk dairy, which should not be homogenized or
have additives like carrageenan, locust bean, guar, etc.).  Make sure
you get enough good quality protein.  Soy, nuts, seeds, beans, etc., is
not going to supply it.  Cheese, eggs, shellfish, milk, and even
potatoes are sources of good quality protein.

DHA and arachidonic acid, for example, are good for emergency medicine.
That is, they are way too powerful for the healthy adult human.  There
is no reason to put rocket fuel in an automobile, but that is similar
to what having more than trace amounts of AA or fish oil do to you.
Stop listening to the hype and start asking for experimental evidence
that is on point.  Do the animals live longer on diet X or diet Y?
Make sure the diets are realistic and that the animals are pumped up
with antioxidants like BHT.  An animals that live a year or so might
get "protection" from BHT, but a human taking it for many years is a
different matter entirely.

Taking "antioxidant supplements" may do more harm than good, so just
stay away from the chemcially unstable substances to begin with.  Below
is an recent abstract that sums up much of what I have been saying on
this newsgroup.  As they say, it's complicated.  Further work needs to
be done, but you can protect your body now by doing the simple things,
as I have outlined above.  Here is a key statement from the abstract
(for those who don't want to read it all):

"...the influence on UV carcinogenesis of both antioxidants has been
reported to diminish as the level of dietary fat decreases, pointing to
the involvement of lipid peroxidative reactions..."
And as I have said, if you pack your body with saturated fatty acids,
such lipid peroxidation will hardly occur.  Your body will make some
Mead acid PUFAs as is necessary, and assuming your diet is decent, you
will have more than enough antioxidant protection, just as our
ancestors did, without taking "supplements."

Integr Cancer Ther. 2004 Dec;3(4):279-93.

Reassessment of a free radical theory of cancer with emphasis on
ultraviolet carcinogenesis.

Black HS.

Department of Dermatology, Baylor College of Medicine, Houston, Texas,
USA. hblack@bcm.tmc.edu

Pro-oxidants, reactive species and free radicals, are toxic substances
that can cause oxidative damage to major constituents of biological
systems. In contradistinction, antioxidants are defined as any
substance that significantly prevents the pro-oxidant-initiated
oxidation of a substrate. Consequently, it was suggested that it might
be possible to reduce free radical damage and thus cancer risk through
3 dietary changes: (1) caloric reduction, that is, lowering the level
of free radical reactions arising in the course of normal metabolism;
(2) minimize dietary components that increase the level of free radical
reactions (eg, polyunsaturated fats); and (3) supplement the diet with
one or more free radical reaction inhibitors (antioxidants). Lipid
peroxidation exemplifies the type of chain reaction initiated by free
radicals in (2) and (3). Both the phenolic antioxidant butylated
hydroxytoluene (BHT) and the carotenoid beta-carotene can terminate
such reactions and have been shown to influence ultraviolet (UV)
carcinogenesis. However, there is a lack of correlation between
physicochemical and patho-physiological responses in both instances.
Whereas the influence on UV carcinogenesis of both antioxidants has
been reported to diminish as the level of dietary fat decreases,
pointing to the involvement of lipid peroxidative reactions, the mode
of BHT's action in inhibiting UV carcinogenesis appears to be related
to UV dose diminution through increased spectral absorbance of the
stratum corneum. beta-carotene has no such effect and may actually
exacerbate UV carcinogenesis under certain dietary conditions. This
paradox points to the complex relationship between chemical mechanisms
and biological mode of action of antioxidants. Recent clinical and
experimental data suggest that antioxidant supplementation of the
complex and intricately balanced natural antioxidant defense system as
a cancer prevention strategy will demand extreme caution.
jaym1212 - 13 Sep 2005 04:04 GMT
> I'm prone to depression so I take about 10 fish oil pills a day...

Could you describe your intake level of omega-6s and their sources?
wizzzer@hotmail.com - 13 Sep 2005 05:51 GMT
I'm not taking omega 6 supplements. That's from flax seeds, isn't it?
I get omega 3 from salmon oil.
Pizza Girl. - 19 Sep 2005 03:28 GMT
Maybe you should consider less of a better quality brand  substance and get
one not containing solvents?

> I'm prone to depression so I take about 10 fish oil pills a day. That's
> 1200 mg of DHA per day, which I think is what is recommended for
> depression. It makes me feel good and my memory has improved too. I get
> the big bottle of 250 pills from Walmart once a month. The Omega 3
> fatty acids enable more serotonin to be created. If I go for a few days
> without the pills, I feel depressed and exhausted.
dali - 13 Sep 2005 04:10 GMT
>Karen Pallarito, "Scientists discover how fish oil protects the brain",
>Cincinnati Enquirer, September 12, 2005,
[quoted text clipped - 4 lines]
>fatty acids found in fish oil help protect the human brain from the
>type of cognitive decline associated with Alzheimer's disease.

great stuff, cannabanoids are also neuroprotective.

It's fine and good to help protect the brain but nothing beats
eliminating the cause of it's destruction.

Spirochetes of unidentified types and strains have previously been
observed in the blood, CSF and brain of 14 AD patients tested and
absent in 13 controls. In three of these AD cases spirochetes were
grown in a medium selective for Borrelia burgdorferi. In the present
study, the phylogenetic analysis of these spirochetes was made.
Positive identification of the agent as Borrelia burgdorferi sensu
stricto was based on genetic and molecular analyses. Borrelia antigens
and genes were co-localized with beta-amyloid deposits in these AD
cases. The data indicate that Borrelia burgdorferi may persist in the
brain and be associated with amyloid plaques in AD. They suggest that
these spirochetes, perhaps in an analogous fashion to Treponema
pallidum, may contribute to dementia, cortical atrophy and amyloid
deposition. Further in vitro and in vivo studies may bring more
insight into the potential role of spirochetes in AD.

PMID: 15665404 [PubMed - indexed for MEDLINE]
montygram - 13 Sep 2005 06:07 GMT
I am confident that reasonable people who still have open minds will be
able to discern what makes the most sense.  I'm sure most people who
read this have relatives like mine.  And it would be nice if you cited
some scientific evidence that was on point.  Everything you cite
assumes the omega 3s and 6s are "essential."  Don't you realize that
you cannot make assumptions that allow you to ignore what you are
trying to demonstrate?  Do you even have a basic understanding of the
scientific method?  Apparently not.

You can cite a million studies, but there needs to be at least one that
establishes the claim in the first place.  In the case of "essential
fatty acids," there was a rat experiment in 1930 that was undeniably
flawed in several ways, and even if it were not, it would only tell us
about rats, which metabolize fats differently anyway (though they still
die of cancer if they eat too much omega 3 and 6 PUFAs).  What that
experiment did show is the following:

If you do not allow rats to have any fatty acids and some truly
essential vitamins and minerals in their diet, they will appear to grow
less quickly and might appear to have mild skin rashes, as well as
other such symptoms.  We have to take the researchers word on this.
These are clinical observations only.  They did not determine if the
fat-free rats lived longer, though other experiments found that the
more unsaturated the fat in the diet, the higher the mortality rates of
the rats.

It was not determined that omega 3 and 6 PUFAs are "essential," but
rather that some amount of fat was, because the researchers assumed
that saturated and monounsaturated fatty acids were not "essential."
This was an assumption that needed to be demonstrated in the experiment
they were doing, and thus the experiment is not to be considered
"scientific."

You say:
"Arachadonate is essential for life. If you're not fed it, you will
make it."

Here, you are making a new claim, one which none of the "experts" agree
with.  All agree that if you avoid omega 6 PUFAs (as I have done for
about 4 years and biochemist Ray Peat has done for a decade or so) you
will not produce AA, but the Mead acid instead.  The Mead acid is
considered a "marker" of "essential fatty acids deficiency."  My
argument is that the Mead acid is involves a greatly attenuated
inflammatory process (something that just about everyone agrees with),
and also that this is best.  Those who disagree state that there is not
enough inflammation generated by the Mead acid, if you are cut, for
example.  I have seen for my own eyes on my own body that this is
false.  Did you see the Charlie Rose Show episode that was dedicated
entirely to the idea that inflammation is the root cause of the
"chronic diseases" of today?  I doubt it, but the point is that if
inflammation is the problem, and that is where the attention is focused
on these days, why not see if a body with Mead acid in it is one that
is healthier?  It can be done on lab animals like dogs (because they
metabolize fatty acids the same as humans).   And then we would know.
The problem, as I have pointed out many times, is that so many
assumptions are now in play that basic science is being ignored.  It's
all about "markers" that are not directly related to the phenomenon as
well as "endpoints" that nobody in his/her right mind would care about.
For example, if you had a tumor, would you rather live a year longer
or would you rather have the tumor shrink 10% more?  The way it works
today, it is often some such ludicdrous "endpoint" that determines the
"success" of a drug, not how long people live.  Side effects of drugs
are almost never taken into account in these kinds of situations,
unless they are literally unbearable.   So it seems you have a bit of
reading to do in order to familiarize yourself with what the issue in
fact is.  If you don't believe me, just go to www.pubmed.com and search
for Mead acid and perhaps mead acid efad or mead acid deficiency.  For
those who have a more scientific background, the following is
excellent:

http://www.fasebj.org/cgi/content/abstract/14/3/532

What is interesting is that some who post here don't realize that there
is one process involved.  For example, MattLB acknowledges that
oxidized cholesterol is the underlying cause of most "heart disease,"
and yet he fails to see that the same process is at work in the other
"chronic disease."  If he did, he would realize that avoiding the oils
that are very biochemically unstable is a way to protect yourself
against this process.  The study at the link I cited explains how
oxidative stress overwhelms the body's ability to deal with the damaged
proteins that result, and then "inflammation" occurs, leading to
"chronic disease."

Eating berries and dark choclate is a good idea, but avoiding highly
unstable substances in your diet is even better.

Still, if you still don't agree with me, take me up on my offer and
"prove" me wrong!

I am still waiting for one of the defenders of the faith to do.  Could
one of you at least explain why you don't want to accept this
challenge?  If you want post on a scientific newsgroup, don't you feel
that you have a responsibility for explaining to those who are reading
this and who are trying to sort it all out why you don't want to
accept?  Such experiments on mice, rats, etc. are done all the time,
and the "essential fatty acid" experiment was done n rats, so there
should be no problem.

They won't accept because they know the mortality of the usual lab
mammals being fed 30% or so of their diet in the form of a mixture of
canola oil and fish oil (from a commercially available source, such as
what you would buy from a retailer) will be unbelievably high.  I would
be surprised if the animals live about half as long as the ones fed
fresh coconut oil.  There will be no way that they can manipulate the
experiment, for example, by giving the animals massive antioxidant
supplements, because I know all the tricks, and these will be
disallowed in the written agreement.  They wil look like fools and be
several thousand dollars poorer.

So what can they do?  They make bad jokes about me and cite irrelevant
studies.  If that passes for science today, those of you who want to
live long, healthy lives had better start thinking and sorting things
out for yourselves, as I had to do when my doctors could not help me,
demonstrating an incredible combination of incompetence and ignorance.
MattLB - 14 Sep 2005 17:29 GMT
> You say:
> "Arachadonate is essential for life. If you're not fed it, you will
> make it."
>
> Here, you are making a new claim, one which none of the "experts" agree
> with.

Nonsense. There's no new claim there and anyone who knows anything
about fatty acid chain elongation would agree with it.

 So it seems you have a bit of
> reading to do in order to familiarize yourself with what the issue in
> fact is.  If you don't believe me, just go to www.pubmed.com and search
[quoted text clipped - 3 lines]
>
> http://www.fasebj.org/cgi/content/abstract/14/3/532

But nothing to do with Mead Acid.

> What is interesting is that some who post here don't realize that there
> is one process involved.  For example, MattLB acknowledges that
> oxidized cholesterol is the underlying cause of most "heart disease,"

No, oxidized LDL is (like the abstract above says).

> and yet he fails to see that the same process is at work in the other
> "chronic disease."

Sorry, which other chronic diseases involve uncontrolled uptake of
oxLDL?

> If he did, he would realize that avoiding the oils
> that are very biochemically unstable is a way to protect yourself
> against this process.

Mead Acid is still a PUFA.

> The study at the link I cited explains how
> oxidative stress overwhelms the body's ability to deal with the damaged
> proteins that result, and then "inflammation" occurs, leading to
> "chronic disease."

The oxLDL toxicity is a specific chemical modification of proteins in
the cell, it's not simply a general oxidative stress. The fact that
blockers of proteasome function speeds up cell death shows that.

> I am still waiting for one of the defenders of the faith to do.  Could
> one of you at least explain why you don't want to accept this
> challenge?  If you want post on a scientific newsgroup, don't you feel
> that you have a responsibility for explaining to those who are reading
> this and who are trying to sort it all out why you don't want to
> accept?

As soon as you explain why you repeated fail to address the studies
showing the essentiality of fatty acids posted by SBHarris and myself
(on dogs and humans) and just go on and on about the same rat study.

MattLB
montygram - 15 Sep 2005 00:52 GMT
Yes, Mead acid is a PUFA - that's the whole point - you make it and it
does the job AA does, only in a much attenutated way.  Even you must
realize that is what will happen.  The only question is whether Mead
acid is not "powerful" enough.  I have had a couple of nasty cuts in
the last year, and they all healed up very nicely, though a bit slower
than in the past.  Don't you realize the implications?  Instead of
taking fish oil to counteract the AA, all one needs to do is to allow
the body to make Mead acid!

And how in the world do those studies SBHarris cites in any way
demonstrate that omega 3s and 6s are essential?  And what about myself,
Ray Peat, and many others I know, some of whom lived to be 100?  The
professional nutritional literature cites the 1930 study, and
everything after that assumed that the 1930 study was correct, so there
is nothing but circular logic involved here.  I have made my points
clearly, inlcuding taking the time to point out exactly what that study
did show.

As to the claim about AA.  My point was that without omega 6s, the body
cannot make AA.  If you have a citation that states otherwise go ahead
and cite it.

You must now realize that your defense of omega 3 and 6 "essentiality"
is beyond ridiculous and so you resort to making statements that lack
scientific sprecifity.  Where is the experiment in which people were
given a fat source like fresh coconut oil, as well as high quality
protein and some carbs, along with basic vitamin and mineral
supplementation, and after x number of years demonstrated signs of
gross deficiency, whereas a control group did not?  It does not exist,
and this is the only experiment that would be on point.

I have offered to pay for a repeat of the 1930 experiment to be done
with proper scientific controls, if your claim is correct.  Why are you
not telling the good people who are reading this your reasons for not
even addressing this offer?

You are a fraud, for whatever reason.  Perhaps you work for a big
pharaceutical company.  I think you said you something to that effect,
but why don't you clarify what your apparent conflicts of interest are?

By contrast, I am only seeking to make sure that the scientific method
is followed before claims are made that will raise cancer rates (and
rates of other "chronic diseases") by motivating people to eat very
dangerous substances.

I will not waste my time responding to you any longer, unless you cite
original experiments that demonstrate the point in contention.  Where
is this experiment for the claim that omega 3s and 6s are "essential?"
Where is the experiment that demonstrated "rapid DHA turnover in the
brain?"  If you are a scientist, don't you realize that this is
physically impossible?  How could people who eat no food source that
has anything but the tiniest amounts of omega 3s, most or all of which
get changed into another molecule during processing, cooking, etc.,
have "rapid DHA turnover?"  Where is the evidence?

In any case, I am still waiting for someone to take me up on my offer.
montygram - 15 Sep 2005 01:07 GMT
And it's not just LDL.  LDL is a form of cholesterol.  You don't even
seem to really understand the points many scientists have made about
oxidized cholesterol.  For example:

Localization of oxidized HDL in atheromatous plaques and oxidized HDL
binding sites on human aortic endothelial cells

Authors: Komoda T.; Nakajima T.; Origuchi N.; Matsunaga T.; Kawai S-i.;
Hokari S.; Nakamura H.; Inoue I.; Katayama S.; Nagata A.

Source: Annals of Clinical Biochemistry, Volume 37, Number 2, 1 March
2000, pp. 179-186(8)

Publisher: Royal Society of Medicine Press
< previous article | next article > View Table of Contents

full text options

Abstract:
We examined the localization of oxidized high-density lipoprotein (HDL)
in atheromatous plaques and the oxidized HDL binding sites on
endothelial cells. Histochemical analysis using CuSO4-oxidized
HDL-specific 9F5-3a antibody indicated the presence of oxidized HDL in
the intima of atheromatous plaques in human abdominal aortae. The cell
surface binding of 125I-oxidized HDL to cultured human aortic
endothelial cells (HAEC) was saturable, with an apparent dissociation
constant (Kd) of 1.43 mol/L. Competition for 125I-oxidized HDL binding
was strong for oxidized HDL, moderate for native HDL and low for
acetylated low-density lipoprotein (LDL) or oxidized LDL. Using
oxidized HDL as a ligand for blotting, a major 130-kDa band was
detected in HAEC. These results suggest that oxidized HDL and its
putative binding protein are present in atheromatous plaques and
endothelial cells, respectively.

And:

Year: 2003 Volume: 2 - Issue: 1

Title:     Potential role of the interaction between equine estrogens,
low-density lipoprotein (LDL) and high-density lipoprotein (HDL) in the
prevention of coronary heart and neurodegenerative diseases in
postmenopausal women
Author:     Perrella Joel; Berco Mauricio; Cecutti Anthony; Gerulath Alan;
Bhavnani Bhagu R
Abstract:

Abstract

Background

An inverse relationship between the level of high-density lipoprotein
(HDL) and coronary heart disease (CHD) has been reported. In contrast,
oxidized HDL (oHDL) has been shown to induce neuronal death and may
play an important role in the pathogenesis of CHD. In the present study
we have investigated a: the effect of various equine estrogens on HDL
oxidation, b: the inhibition of LDL oxidation by HDL and c: the effect
of these estrogens on LDL oxidation in the presence of HDL.

Results

All 11 equine estrogens tested protected the HDL from oxidation in a
concentration dependant manner. Equilenin, 17-dihydroequilenin, and
17-dihydroequilenin (68-estrogens) were found to be the most
potent inhibitors of HDL oxidation. Some of the novel ring B
unsaturated estrogens were 2.5 to 4 times more potent inhibitors of HDL
oxidation than 17-estradiol. HDL was found to delay LDL oxidation.
The protection of LDL oxidation by HDL is enhanced by the addition of
estrogen, with equilenin being again more potent than 17-estradiol.

Conclusions

Equine estrogens can differentially inhibit the oxidation of HDL with
the 68-estrogens being the most potent antioxidants. The ability
of estrogens to enhance HDL's antioxidant activity is to our knowledge
the first report of an interaction of estrogen with HDL that results in
the delay or inhibition of LDL oxidation. This may be another mechanism
by which estrogens may reduce the risk of CHD and neurodegenerative
diseases in healthy and younger postmenopausal women.
Journal:     Lipids in Health and Disease

A key statment they make:
"
HDL was found to delay LDL oxidation."

Notice that they support my point, namely, that oxidative stress is the
key to "chronic disease," though I have made it clear time and time
again that Denham Harman was first, in the 1970s.  This is not new, but
now the evidence is overwhelming, and eating food that is unstable and
highly likely to cause oxidative stress is beyond stupid.

There are plenty more, so why don't you do some reading before you tell
people to eat dangerous foods?  Start with this one:

Hurtado, I., Fiol, C., Gracia, V., and Caldu, P. (1996).
"In vitro oxidized HDL exerts a cytotoxic effect on macrophages."
Atherosclerosis 125, 39-46.

Or perhaps this one:

The role of oxidized HDL in monocyte/macrophage functions in the
pathogenesis of atherosclerosis in Rhesus monkeys

Authors: Sharma N; Desigan B; Ghosh S; Sanyal S. N; Ganguly N. K;
Majumdar S

Source: Scandinavian Journal of Clinical and Laboratory Investigation,
Volume 59, Number 3, 11 June 1999, pp. 215-225(11)

Publisher: Taylor and Francis Ltd
< previous article | next article > View Table of Contents

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Abstract:
The effect of oxidative modification of high-density lipoprotein (HDL)
was assessed by incubation of normal HDL (obtained from Rhesus monkeys
fed a stock diet) with 5 M CuSO4 at 37=B0C for 12 h/24 h. The
physicochemical properties of oxidized-HDL (Ox-HDL) were found to be
affected in terms of lipid peroxidation, as observed by the increased
level of thiobarbituric acid reactive substances (nmol MDA/mg HDL
protein). The biological properties of HDL were altered, since a
decrease in the efflux of free cholesterol into the medium was found in
the presence of Ox-HDL24h compared with normal HDL (N-HDL). The
binding, uptake and degradation of 125I-LDL by macrophages increased in
the presence of Ox-HDL24h. The activity of antioxidant enzymes
(superoxide dismutase, catalase and glutathione-peroxidase) was reduced
in monocytes in the presence of Ox-HDL. However, in the presence of
N-HDL, the levels of antioxidant enzymes were maintained at a higher
level than in the control (in the absence of HDL) monocytes.
Furthermore, the number of monocytes adhered to aortic endothelium were
found to be increased in the presence of Ox-HDL. These findings suggest
that HDL is susceptible to oxidative modification. Since the parameters
selected in the present study are involved in the pathogenesis of
atherosclerosis, it can be postulated that the in vivo protection of
HDL in atherosclerosis can be reversed in the circumstances in which
HDL undergoes oxidative modification like low-density lipoprotein
(LDL).
MattLB - 15 Sep 2005 17:23 GMT
> And it's not just LDL.  LDL is a form of cholesterol.

No it isn't. LDL is low density lipoprotein, a protein that transports
a mixture of triglycerides, cholesterol/cholesterol esters and
phospholipids in the blood. It happens to have the highest
concentration of cholesterol of all the lipoproteins, but that's the
closest it is to *being* cholesterol.

>  You don't even
> seem to really understand the points many scientists have made about
> oxidized cholesterol.

One minute you're using me as support for your viewpoint, the next I
supposedly don't understand a thing.

> For example:
> Localization of oxidized HDL in atheromatous plaques and oxidized HDL
> binding sites on human aortic endothelial cells

Yes, so? HDL removes cholesterol from extrahepatic sites. That it
should have binding sites in plaques is not that surprising. Since HDL
has the lowest cholesterol content of all the lipoproteins, it's a bad
choice for your "it's all about oxidised cholesterol" theory. It's
oxidation of the protein that causes the problems and alters the
behaviour of the lipoprotein.

> Title:     Potential role of the interaction between equine estrogens,
> low-density lipoprotein (LDL) and high-density lipoprotein (HDL) in the
> prevention of coronary heart and neurodegenerative diseases in
> postmenopausal women

> A key statment they make:
> "
> HDL was found to delay LDL oxidation."

Again, so? HDL and LDL both have fatty acids in them. HDL can stop
oxidation of LDL (fatty acids and all), so maybe the fatty acids aren't
the most important thing. The paper says nothing to support your
anti-PUFA viewpoint. It merely  points out that by acting as an
antioxidant oestrogens can stop oxidation of HDL, which can stop
oxidation of LDL.

> There are plenty more, so why don't you do some reading before you tell
> people to eat dangerous foods?  Start with this one:
>
> Hurtado, I., Fiol, C., Gracia, V., and Caldu, P. (1996).
> "In vitro oxidized HDL exerts a cytotoxic effect on macrophages."
> Atherosclerosis 125, 39-46.

In vitro oxidation is always done with free metal ions. They don't just
add some fatty acids. What they've found is basically: "exposing HDL to
high metal ion concentrations damages the protein in a way that makes
it toxic to macrophages"

> The role of oxidized HDL in monocyte/macrophage functions in the
> pathogenesis of atherosclerosis in Rhesus monkeys

None of these support your attack on fatty acids. They are all saying
that oxidised proteins have abnormal effects. Even if you had some LDL
or HDL containing no PUFA at all (and they always will even if it's
only Mead Acid) the cholesterol and protein could still be oxidised.

Yes, uncontrolled oxidation of cell components is a bad thing, no-one's
ever doubted that. Oxidative stress is bad thing, no-one's suggesting
it isn't. Trying to claim it's all the fault of omega3/6 and that none
of it happens with Mead Acid is just deluded.

MattLB
montygram - 16 Sep 2005 02:13 GMT
To Mattia:

I agree totally.  So what is your explanation about me still being
alive?  My contention is that these metabolites are not necessary, but
usually harmful, especially as one ages.  Where is the evidence that I
am going to harm myself?

To MattLB:

I never saw your response.

Are you accepting my offer to repeat the 1930 experiment, only without
the assumption that SFAs and MUFAs are not essential?

If not, why not?  It is the only on point experiment, though they began
with faulty assumptions that were only ideas up to that point.  If it
is ridiculous, then how much more ridiculous is it that the same
experiment, except done without proper controls, is still being cited?
Do you agree with Burr & Burr, 1930, or do you not?

I've read all the citations you listed already.  None are on point.

What are you trying to say about DHA "turnover."  I did not make any
claims.  It is up to those who make the claims to do the explaining, as
I always do.  If by "turnover," it is meant that the DHA is present at
birth and keeps getting broken down and then remade, there is no need
to worry that one will be deficient in it (if it was in fact
"essential").

I agree, and have made the point, that the body will not make omega 3s
and 6s without dietary input - that is my whole point.  It is better
not to eat such PUFAs.  And what are theses studies supposed to mean,
in the case of someone like myself, who avoids any food that has more
than trace amounts of omega 3s and 6s?  What should happen to me, now
that I'm 4 years into this experiment of mine?  What about Ray Peat, a
man in his late 60s or so, who has done this for about a decade?

Explain yourself, as I do, or else there is nothing for me to respond
to.

As I've said, with Mead acid, the responses are greatly attenuated
(compared to AA or EPA & DHA).  I've been very clear on that point.
Are you reading the posts or not?

About my offer you say:

"And you really can't see why it [somebody accepting] won't happen?"

Again, I am proposing to repeat the 1930 experiment, only in the
repeat, we will not make any assumptions about which fatty acids are
essential and which ones are not.  We will let the experimental results
tell us, as is consistent with the scientific method.  Allowing
notions that sound good to you to  dictate how you will set up your
experiment, rather than using proper scientific controls is
unscientific.  

And you really can't understand this?
montygram - 16 Sep 2005 02:53 GMT
As for the tangential points:

"What the study quoted shows is that you can give
dogs atherosclerosis feeding them coconut oil, but if you give them
safflower oil instead they don't get it."

This does not mean the dogs that are getting the safflower oil are
living longer.  You should know that.  If you want to take me up on an
offer to repeat this experiment, with me supplying the coconut oil (and
proper controls being used), along with the obvious relevant result
(mortality) being the "endpoint," as they say these days, then just
give me the name of your lawyer and let's get the ball rolling.

As for the "cholesterol" points, there is now plenty of evidence that
is direct and explained well.  For example:

J Lipid Res. 2004 Apr 1 [Epub ahead of print]
The oxidation hypothesis of atherogenesis: The role of oxidized
phospholipids and HDL.

Navab M, Anantharamaiah GM, Reddy ST, Van Lenten BJ, Ansell BJ, Fonarow
GC, Vahabzadeh K, Hama SY, Hough GP, Kamranpour N, Berliner JA, Lusis
AJ, Fogelman AM.

For more than two decades, there has been continuing evidence of lipid
oxidation playing a central role in atherogenesis. The oxidation
hypothesis of atherogenesis has evolved to focus on specific
pro-inflammatory oxidized phospholipids, which result from the
oxidation of LDL phospholipids containing arachidonic acid, and which
are recognized by the innate immune system in animals and humans. These
oxidized phospholipids are largely generated by potent oxidants
produced by the lipoxygenase and myeloperoxidase pathways. The failure
of anti-oxidant vitamins to influence clinical outcomes may have many
explanations including the inability of vitamin E to prevent the
formation of these oxidized phospholipids and other lipid oxidation
products of the myeloperoxidase pathway. Preliminary data suggest that
the oxidation hypothesis of atherogenesis and the reverse cholesterol
transport hypothesis of atherogenesis may have a common biological
basis. The levels of specific oxidized lipids in plasma and
lipoproteins, the levels of antibodies to these lipids, and the
inflammatory/anti-inflammatory properties of HDL may be useful markers
of susceptibility to atherogenesis. ApoA-I and apoA-I mimetic peptides
may promote both a reduction in oxidized lipids and enhance reverse
cholesterol transport and therefore may have therapeutic potential.

What is needed is to do an experiment to see how much more resistant to
oxidative stress the lipoproteins would be if they contained Mead acid
instead of AA.  It's a matter or how much, not if, because all agree
that Mead acid is much more stable than AA.

The cytotoxic effects of a high PUFA diet (in the carcinogenic context)
are best explained by Gower:

Title: A role for dietary lipids and antioxidants in the activation of
carcinogens.
Author(s): Gower JD
Address: Division of Comparative Medicine, Clinical Research Centre,
Harrow, Middlesex, U.K.
Source: Free Radic Biol Med 1988;5(2):95-111
Abstract: The ways in which dietary polyunsaturated fats and
antioxidants affect the balance between activation and detoxification
of environmental precarcinogens is discussed, with particular reference
to the polycyclic aromatic hydrocarbon benzo(a)pyrene. The structure
and composition of membranes and their susceptibility to peroxidation
is dependent on the polyunsaturated fatty acid (PUFA) content of the
cell and its antioxidant status, both of which are determined to a
large degree by dietary intake of these compounds. An increase in the
PUFA content of membranes stimulates the oxidation of precarcinogens to
reactive intermediates by affecting the configuration and induction of
membrane-bound enzymes (e.g., the mixed-function oxidase system and
epoxide hydratase); providing increased availability of substrates
(hydroperoxides) for peroxidases that cooxidise carcinogens (e.g.,
prostaglandin synthetase and P-450 peroxidase); and increasing the
likelihood of direct activation reactions between peroxyl radicals and
precarcinogens. Antioxidants, on the other hand, protect against lipid
peroxidation, scavenge oxygen-derived free radicals and reactive
carcinogenic species. In addition some synthetic antioxidants exert
specific effects on enzymes, which results in increased detoxification
and reduced rates of activation. The balance between dietary
polyunsaturated fats, antioxidants and the initiation of carcinogenesis
is discussed in relation to animal models of chemical carcinogenesis
and the epidemiology of human cancer.

I'm not sure what MattLB is suggesting, in the "big picture," so I will
ask the following questions, and we will see if he responds directly or
not:

1. Exactly what is going to happen to a person who eats according to
nutritional guidelines with the exception of avoiding all major sources
of omega 3 and 6 PUFAs?
And if there are "negative effects," why have I and others only
experienced positive one?

2.  Do you think it is very likely that Americans, in general, are
subjecting themselves to more oxidative stress than is healthy by
consuming foods high in PUFAs?  Remember, most Americans do not have
high levels of antioxidant-rich foods, and we cannot assume that they
will change this dietary choice any time soon.

3.  Do you see the connection between a "typical American diet" and
cholesterol oxidation?  If so, what is it?

4.  Do you recognize the basic chemical laws that suggest that if you
compare a highly unsaturated oil to a highly saturated one in a
biological context (all things being equal, such as antioxidant content
of the oils), the highly unsaturated one will produce more oxidative
stress on the organism than the highly saturated one, if the organism
is not being supplied with antioxidant supplementation?

If you answer these questions directly, and they are different from the
answers I would give, then you are at odds with the scientists who have
studied the phenomena directly, as opposed to those who start with
assumptions that were never verified by legitimate experiments (that
is, those that use the scientific method), then look for "markers" and
"associations" of epiphenomenal effects.

I am waiting...
MattLB - 19 Sep 2005 14:01 GMT
> As for the tangential points:
>
[quoted text clipped - 4 lines]
> This does not mean the dogs that are getting the safflower oil are
> living longer.

Where does living longer come into it? It's talking about getting or
not getting atherosclerosis. Atherosclerosis is clearly one of the
chronic diseases you're always blaming omega 6 for.

> As for the "cholesterol" points, there is now plenty of evidence that
> is direct and explained well.  For example:
>
> J Lipid Res. 2004 Apr 1 [Epub ahead of print]
> The oxidation hypothesis of atherogenesis: The role of oxidized
> phospholipids and HDL.

Interesting, but it doesn't disagree with, or answer, anything I said.

> What is needed is to do an experiment to see how much more resistant to
> oxidative stress the lipoproteins would be if they contained Mead acid
> instead of AA.  It's a matter or how much, not if, because all agree
> that Mead acid is much more stable than AA.

As long as you have your own vague use of "stable" it's hard to
comment, but in terms of free radical propagation Mead acid will do it
just fine. Offhand I don't know what specificity the oxygenases have,
so whether they act on omega 9 like Mead acid I don't know.

> The cytotoxic effects of a high PUFA diet (in the carcinogenic context)
> are best explained by Gower:

As long as it's just "PUFA" i.e. a chemical issue rather than
biochemical, it applies to Mead acid too.

> 1. Exactly what is going to happen to a person who eats according to
> nutritional guidelines with the exception of avoiding all major sources
> of omega 3 and 6 PUFAs?

The same things that the intravenous nutrition studies I've quoted over
and over say. You have the qualifier of "major" I see. That means that
a person may not be deficient as they are getting little bits from a
variety of poor sources.

> And if there are "negative effects," why have I and others only
> experienced positive one?

You're not avoiding them as well as you think, or you've accumulated a
lot previously.

> 2.  Do you think it is very likely that Americans, in general, are
> subjecting themselves to more oxidative stress than is healthy by
> consuming foods high in PUFAs?  Remember, most Americans do not have
> high levels of antioxidant-rich foods, and we cannot assume that they
> will change this dietary choice any time soon.

Yes, most people probably have poor diets that involving cooking with
heat-sensitive oils and are doing themselves harm in the process. I've
said before that this aspect isn't controversial.

> 3.  Do you see the connection between a "typical American diet" and
> cholesterol oxidation?  If so, what is it?

Cooking oxidises food.

> 4.  Do you recognize the basic chemical laws that suggest that if you
> compare a highly unsaturated oil to a highly saturated one in a
> biological context (all things being equal, such as antioxidant content
> of the oils), the highly unsaturated one will produce more oxidative
> stress on the organism than the highly saturated one, if the organism
> is not being supplied with antioxidant supplementation?

Unsaturated fatty acids are more susceptible to free radical attack.
Again nothing controversial there.

MattLB
montygram - 16 Sep 2005 06:53 GMT
One point I made that suggests strongly that you read my posts in a
selective manner concerns experiments such as the dog/safflower/coconut
oil experiment.  Do you know if the dogs were force fed the safflower
oil, or was the food just left in the cage?  If it was left in the cage
and thrown out at a certain time if the dogs did not eat it, then it
was really a study of calorie restricted dogs verus dogs fed
poor-quality coconut oil.  Remember that many researchers who do, or
have done, these studies do not understand the implications the
implications of rancid fat, so it may be unintentional on their part.

Here's a good example of the importance of this point:  I had an old
jar of mediocre-quality coconut oil, and I then purchased another brand
which I could taste was better/fresher.  I forgot about the first jar,
but then found it again several months later.  I could smell it was
going  bad, but I decided to smear a little on a biscuit I give to my
dog.  When this coconut oil was first purchased, the dog ate the
biscuit smeared with the coconut oil as quickly as he could, but when I
smeared it on after it had gone bad, he turned his head when I put it
in front of his face.  Even after taking most of it off, he still
wouldn't eat it.  I had to scrape off every trace of the bad coconut
oil, and then he ate it. Thus, the experiment may have only
demonstrated that a lot of very "intelligent" scientists have little
common sense at times.

Also, how many dogs die of heart attacks?  There have been many dogs
owned in my family, and I've known many of my neighbors dogs fairly
well over the years.  None died of heart attacks.  Do you realize what
a ridiculous model this is?

And has a baseline for dog atherosclerosis been established, so that
the atherosclerosis they measured should correspond to significantly
higher mortality than dogs will less plaque buildup?  If not, how would
they know if it was not actually an enhancer of dog life expectancy?

The problem seems to be that you don't mind accepting all kinds of
assumptions if a researcher makes a claim that you would like to agree
with, yet when someone makes a claim you do not like the sound of, you
will pull out many citations that are flawed badly, are not on point,
are based on assumptions now known to be false, or do not provide
enough information to know exactly what they did or what materials they
used.  For example, a rancimat test should be used in a fat/oil
experiment to ensure that the oil is fresh.

The "bottom line" is that when a study comes to a conclusion that makes
no sense in terms of basic scientific laws (such as this dog study that
suggests that a highly saturated fat source generates more oxidative
stress than a highly unsaturated fat source), one should investigate
and determine if the experiment was conducted properly.  No scientist
should criticize this.  In fact, scientists should welcome such
investigation with open arms.  However, for someone selling flax oil,
or fish oil, or expensive new drugs, or "supplements," there is a real
threat to them.

Thus, I make my offer to the "true believers" of the "benefits" of
highly unsaturated oils.  If the animals are not force fed, nor given
massive antioxidant supplements, and if fresh coconut oil is used, and
if mortality is the "endpoint," the animals fed the highly unsaturated
oils will die much sooner, even though you "true believers" think that
they will live much longer.  So why not accept my challenge?  We will
do the experiment properly, making sure that there are no flaws in it.

And that is why you won't accept my challenge - you know that without
being able to manipulate it, the experiment will demonstrate not only
that you are wrong, but that you are badly wrong.
MattLB - 20 Sep 2005 13:05 GMT
> One point I made that suggests strongly that you read my posts in a
> selective manner concerns experiments such as the dog/safflower/coconut
[quoted text clipped - 5 lines]
> have done, these studies do not understand the implications the
> implications of rancid fat, so it may be unintentional on their part.

I assume you've been struggling to come up with an explanation for the
results as this is rather desperate. It seems very unlikely that the
researchers gave the dogs a little bowl of each of the components as
you seem to be suggesting. Rather there would just be a bowl of dog
food made by mixing up all the components. The dogs wouldn't know what
oil was being eaten.

> Here's a good example of the importance of this point:  I had an old
> jar of mediocre-quality coconut oil, and I then purchased another brand
[quoted text clipped - 10 lines]
> demonstrated that a lot of very "intelligent" scientists have little
> common sense at times.

That's a funny story.

> Also, how many dogs die of heart attacks?  There have been many dogs
> owned in my family, and I've known many of my neighbors dogs fairly
> well over the years.  None died of heart attacks.  Do you realize what
> a ridiculous model this is?

That's the whole point. Dogs don't get it normally. Just like if you
feed rabbits oxidised cholesterol they get atherosclerosis where they
don't normally.

> The problem seems to be that you don't mind accepting all kinds of
> assumptions if a researcher makes a claim that you would like to agree
[quoted text clipped - 3 lines]
> enough information to know exactly what they did or what materials they
> used.

Once again you say more about yourself with these statements than the
people who disagree with you.

>For example, a rancimat test should be used in a fat/oil
> experiment to ensure that the oil is fresh.

But then it wouldn't be like the real world where people don't eat
analytical grade coconut oil.

> The "bottom line" is that when a study comes to a conclusion that makes
> no sense in terms of basic scientific laws (such as this dog study that
> suggests that a highly saturated fat source generates more oxidative
> stress than a highly unsaturated fat source),

You're too hung up on oxidative stress being the cause of everything.
It's about atherosclerosis being increased. There are many reasons that
can happen.

> Thus, I make my offer to the "true believers"

With which you demonstrate clearly your inability to recognise that you
are the one with a belief system of nutrition, not us.

MattLB
Juhana Harju - 15 Sep 2005 06:15 GMT
: Yes, Mead acid is a PUFA - that's the whole point - you make it and it
: does the job AA does, only in a much attenutated way.  Even you must
[quoted text clipped - 4 lines]
: taking fish oil to counteract the AA, all one needs to do is to allow
: the body to make Mead acid!

There are multiple advantages in taking fish oils, not only to reduce
inflammation by regulating eicosanoid production. Fish oils prevent fatal
cardiac arrhytmias, reduce clotting and the risk of thrombosis, enhance
cognitive functions -- to name just few advantages of taking fish oils. They
have also been shown to reduce total mortality.

--
Juhana
Matti Narkia - 15 Sep 2005 12:11 GMT
14 Sep 2005 16:52:31 -0700 in article
<1126741951.749638.215400@g43g2000cwa.googlegroups.com> "montygram"
<nazztrader@lycos.com> wrote:

>Yes, Mead acid is a PUFA - that's the whole point - you make it and it
>does the job AA does, only in a much attenutated way.

Only in your dreams. Many eicosanoids such as prostacyclin, thromboxane,
leukotrienes and many prostaglandins are made from arachidonic acid. Humans
cannot make them from mead acid.

> Even you must
>realize that is what will happen.  The only question is whether Mead
[quoted text clipped - 3 lines]
>taking fish oil to counteract the AA, all one needs to do is to allow
>the body to make Mead acid!

Even how much you try to avoid omega-6 fatty acids, you will still get some
from your diet and consequently have also arachidonic acid in your body,
although less than people in average. I think that the only way to avoid
getting omega-6s is an artificial diet where you eat only purified nutriens
such as free form amino acids, free fatty acids (excluding omega-6s),
purified carbohydrate like sugar (perhaps carbohydrates are not neceeary,
because so far they have not been shown to be essential for humans),
vitamins, minerals and trace-elements. But I doubt that you would be able to
survive with this kind diet, even if it included omega-6s. Without omega-6s
you are doomed.

Signature

Matti Narkia

MattLB - 15 Sep 2005 16:51 GMT
> Yes, Mead acid is a PUFA - that's the whole point

The point is any claims you make about omega 6/3 being unstable and
causing oxidative stress also apply to Mead Acid. Mead Acid will
propagate a free radical chain reaction just as readily as any other
PUFA, so you can't claim your no omega3, no omega 6 diet means less
free radicals.

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

As I've said before essential in the context of fatty acids means
"unable to synthesize them from scratch", it doesn't mean "a quick
death without them". What the study quoted shows is that you can give
dogs atherosclerosis feeding them coconut oil, but if you give them
safflower oil instead they don't get it.

A quote from the abstract:

" 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"

Whinge about it being hydrogenated coconut oil and not the same
free-range pressed-that-day organic stuff you buy, all you want, but
I've already pointed out the flaw in that.

> I have made my points
> clearly, inlcuding taking the time to point out exactly what that study
> did show.

Funny there's no reply from you I can see.

> As to the claim about AA.  My point was that without omega 6s, the body
> cannot make AA.  If you have a citation that states otherwise go ahead
> and cite it.

He didn't say without omega 6, so you were protesting a claim that was
never made.

> You must now realize that your defense of omega 3 and 6 "essentiality"
> is beyond ridiculous and so you resort to making statements that lack
> scientific sprecifity.

Is that supposed to be "specificity"? If so you've got it completely
backwards. You're the one using "essential" in some vague unscientific
way. Your detractors are using it in the precise biochemical sense.

>  Where is the experiment in which people were
> given a fat source like fresh coconut oil, as well as high quality
> protein and some carbs, along with basic vitamin and mineral
> supplementation, and after x number of years demonstrated signs of
> gross deficiency, whereas a control group did not?  It does not exist,
> and this is the only experiment that would be on point.

The presence or absence of coconut oil is irrelevant if your claim is
that it is the absence of omega 3/6 that's important.

> I have offered to pay for a repeat of the 1930 experiment to be done
> with proper scientific controls, if your claim is correct.  Why are you
> not telling the good people who are reading this your reasons for not
> even addressing this offer?

1) I've done so before
2) It was ridiculous then and is still ridiculous now.

> You are a fraud, for whatever reason.  Perhaps you work for a big
> pharaceutical company.  I think you said you something to that effect,

No, but you've convinced yourself I've said all sorts of things in the
past, so don't stop now.

> but why don't you clarify what your apparent conflicts of interest are?

I have none.

> I will not waste my time responding to you any longer, unless you cite
> original experiments that demonstrate the point in contention.  Where
> is this experiment for the claim that omega 3s and 6s are "essential?"

Okay, outing number seven for this I think. In case it's not clear EFAD
stands for essential fatty acid deficiency.

"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 for proving that your body lacks the enzymes to make omega 3 and 6
itself (the strict definition of essentiality) that's so easy you
probably couldn't get a paper published on it these days.

> Where is the experiment that demonstrated "rapid DHA turnover in the
> brain?"  If you are a scientist, don't you realize that this is
> physically impossible?

Every molecule in the body is turned over. Why should DHA be any
different? What is your understanding of what "turnover" means?

>  How could people who eat no food source that
> has anything but the tiniest amounts of omega 3s, most or all of which
> get changed into another molecule during processing, cooking, etc.,
> have "rapid DHA turnover?"  Where is the evidence?
>
> In any case, I am still waiting for someone to take me up on my offer.

And you really can't see why it won't happen?

MattLB
Sbharris[atsign]ix.netcom.com - 16 Sep 2005 21:25 GMT
> 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
montygram - 17 Sep 2005 02:28 GMT
It makes sense that cells grown under particular in vitro circumstances
would need the extra "boost" from the more biochemically active omega
3s and 6s.  Do you have a citation so that I can examine exactly how
the experiment was conducted?  Someone posted a study that claimed that
certain kinds of tumor cells did grow in vitro with Mead acid, but they
didn't compare this to AA, which likely would have shown that the AA
helped the cells grow much faster.

But again, my point is that a grown human wants very little biochemical
activity, and so the Mead acid is best.  There are thresholds for
growth which vary from cell type to cell type, species to species, etc.
If omega 6s and/or 3s are truly as essential as you claim, the
experiments I've been proposing would make this very clear.

None of this talk, though, explains the claim about needing both AA and
EPA,DHA, or some combination.  From observing the lives of my older
relatives, it is clear that this claim is total nonsense.

Nor are the studies that demonstrate clear benefit from Mead acid, in
several in vivo contexts, ever addressed by people like you.  And of
course you avoid all the evidence I've presented that suggests that AA
is to chemically unstable in organims like humans, and all the evidence
linking AA to every "chronic disease" that exists.  In light of the
evidence, whether you want to address it or not, it would seem that
doing such a cheap, simple experiment would be of great benefit to
mankind, if indeed it turned out that animals fed only fresh coconut
oil as their fat source remained active and vital into old age and
lived much longer than animals fed  25-20% of their caloric intake from
acanola/fish oil combination.  Then, it may be that my claim that AA