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| montygraham... |
 Posted: Fri Nov 06, 2009 5:48 pm |
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I think we need a feature here that is similar to his "candidates" for
"The Worst Person in the World.:
My nomination is the one with the title of the report: How Saturated
Fatty Acids 'Anger' The Immune System (And How To Stop Them).
The only statement in that report about dietary effects is the
following:
"Mice lacking Tlr4 only in blood cells grew obese when they were fed a
high-fat diet..."
Obviously, this does not mean the diet was rich in saturated fatty
acids. In fact, of all the people I know well, I am the only one who
has a diet that is comprised of more than 50% saturated fatty acids
(in my case, a lot more than 50%). Have these "scientists" actually
done any research into studies or experiments that already examined
this notion? It doesn't appear to be the case. If they did, they
would have seen ones like:
Immunology. 1999 March; 96(3): 404-410.
Abstract: To investigate the effect of dietary lipids with different
fatty acid compositions upon the in vivo cytokine response to
bacterial lipopolysaccharide (LPS), mice were fed for 5 weeks on a low-
fat diet or on one of four high-fat diets that contained 20%, by
weight, of coconut oil (CO), olive oil (OO), safflower oil (SO) or
fish oil (FO). The mice were injected intraperitoneally with a non-
lethal dose of Escherichia coli LPS (100 ìg/20 g body weight) and
killed 90 or 180 min later. Plasma tumour necrosis factor-á (TNF-á),
interleukin (IL)-1á, IL-6 and IL-10 concentrations were measured by
enzyme-linked immunosorbent assay (ELISA). Plasma TNF-á and IL-10
concentrations were higher 90 min postinjection than after 180 min,
whereas plasma IL-1â and IL-6 concentrations were higher 180 min
postinjection than after 90 min. Peak plasma TNF-á, IL-1â and IL-6
concentrations were lower in the CO- and FO-fed mice than in those fed
the SO diet. Peak plasma IL-10 concentrations were higher in CO-fed
mice than in those fed some of the other diets. These observations
suggest that, relative to the n-6 polyunsaturated fatty acid-rich SO
diet, CO and FO diminish production of proinflammatory cytokines in
vivo. This indicates that these fatty acids might be useful therapies
in acute and chronic inflammatory diseases. The enhanced production of
IL-10 following CO feeding appears to be an additional
antiinflammatory effect of this oil, which could give added benefit in
various clinical conditions.
J Am Coll Cardiol. 2006 Jun 20;47(12):2436-43.
Abstract: Oxidized low-density lipoprotein autoantibodies, chronic
infections, and carotid atherosclerosis in a population-based study.
Mayr, M., et al. OBJECTIVES: We investigated whether associations
exist between immune reactions to oxidized low-density lipoproteins
(OxLDLs), chronic infections, and carotid atherosclerosis as
quantified by ultrasound. BACKGROUND: Atherosclerosis is a chronic
immuno-inflammatory disease wherein both oxidized lipids and
infectious agents are incriminated as possible contributors. METHODS:
We measured immunoglobulin (Ig)G and IgM autoantibody titers to copper-
oxidized-LDL and malondialdehyde-LDL (OxLDL-AB), IgG and IgM
apolipoprotein B-100-immune complexes (ApoB-IC), and titers of
antibodies to Escherichia coli and chlamydial lipopolysaccharide
(LPS), mycobacterial heat shock protein 65 (mHSP65), Chlamydia
pneumoniae, Helicobacter pylori, and cytomegalovirus and evaluated
their relationship to cardiovascular risk factors, chronic infections,
and incident/progressive carotid atherosclerosis in the Bruneck study.
RESULTS: The OxLDL-AB and ApoB-IC levels remained stable over time as
indicated by strong correlations between 1995 and 2000 measurements (p
< 0.001 each). Significant associations existed between all OxLDL
markers and antibody titers to pathogens, especially to E. coli-LPS
and mHSP65. Both OxLDL-AB and ApoB-IC levels showed a rise with
increasing pathogen burden. Notably, OxLDL-ABs were also elevated in
subjects with chronic infection as defined by clinical criteria.
Titers of IgG, but not IgM, OxLDL-AB, or ApoB-IC inversely correlated
with total cholesterol, LDL cholesterol, and apoB concentrations. The
IgG OxLDL markers were positively and IgM markers were inversely
associated with incident and progressive carotid atherosclerosis in
univariate analyses but were not independent predictors in
multivariate analyses. CONCLUSIONS: Our study provides evidence for an
association between human oxLDL markers and chronic infections.
Moreover, in this population-based study, neither IgG nor IgM OxLDL
autoantibodies were independently predictive of atherosclerosis
progression in the carotid arteries.
So, how could scientists be this "out of touch?" It may just be that
the author is the one who is badly misinformed, but they are supposed
to have strong scientific backgrounds. The author also made this
statement:
"Researchers have new evidence to explain how saturated fatty acids,
which soar in those who are obese..."
What does that even mean? It's possible that those classified as
obese have higher TG levels, but that does not mean that the SFA
content is higher in those TGs. It may even be lower. Whether the
author realizes it or not, this kind of "report" serves a propaganda
function and may cost many people their lives. |
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| montygraham... |
| Posted: Fri Nov 06, 2009 6:05 pm |
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Though I've pointed it out before, these kinds of statements are
scientifically impossible:
"Researchers have new evidence to explain how saturated fatty acids,
which soar in those who are obese, can lead the immune system to
respond in ways that add up to chronic, low-grade inflammation..."
SFAs can only inhibit inflammation. PUFAs are used for "inflammatory"
purposes. In most "Westerners" these days, arachidonic acid (an omega
6 PUFA) is used to generate inflammation. This is biochemistry at the
most basic level imaginable. If someone does not know this, I can't
imagine why any credible organization would allow that person to write
"science reports." |
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| Taka... |
| Posted: Sat Nov 07, 2009 6:25 am |
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Guest
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On Nov 7, 1:05 pm, montygraham <monty1... at (no spam) lycos.com> wrote:
[quote]Though I've pointed it out before, these kinds of statements are
scientifically impossible:
"Researchers have new evidence to explain how saturated fatty acids,
which soar in those who are obese, can lead the immune system to
respond in ways that add up to chronic, low-grade inflammation..."
SFAs can only inhibit inflammation. PUFAs are used for "inflammatory"
purposes. In most "Westerners" these days, arachidonic acid (an omega
6 PUFA) is used to generate inflammation. This is biochemistry at the
most basic level imaginable. If someone does not know this, I can't
imagine why any credible organization would allow that person to write
"science reports."
[/quote]
I would call this the "The Dark Ages" in nutritional sciences. Will
ever the Enlightenment come? Scientists are so specialized and
concerned more about money and personal careers than anything else
that they can never interconnect the information from immunology,
molecular pathology, organic chemistry and nutrition. Parroting the
established dogmas and popular opinion like a bible is the
mainstream. They will never run out of new inhibitors of chronic
inflammation. And the peer review system has turned into business as
well otherwise papers like this can never be published in the prestige
EMBO Journal:
EMBO J. 2008 Sep 3;27(17):2281-92.
Delta6-desaturase (FADS2) deficiency unveils the role of omega3- and
omega6-polyunsaturated fatty acids.
Stoffel W, Holz B, Jenke B, Binczek E, Günter RH, Kiss C,
Karakesisoglou I, Thevis M, Weber AA, Arnhold S, Addicks K.
Center of Molecular Medicine (CMMC), Laboratory of Molecular
Neurosciences, Institute of Biochemistry, University of Cologne,
Cologne, Germany.
Mammalian cell viability is dependent on the supply of the essential
fatty acids (EFAs) linoleic and alpha-linolenic acid. EFAs are
converted into omega3- and omega6-polyunsaturated fatty acids (PUFAs),
which are essential constituents of membrane phospholipids and
precursors of eicosanoids, anandamide and docosanoids. Whether EFAs,
PUFAs and eicosanoids are essential for cell viability has remained
elusive. Here, we show that deletion of delta6-fatty acid desaturase
(FADS2) gene expression in the mouse abolishes the initial step in the
enzymatic cascade of PUFA synthesis. The lack of PUFAs and eicosanoids
does not impair the normal viability and lifespan of male and female
fads2 -/- mice, but causes sterility. We further provide the molecular
evidence for a pivotal role of PUFA-substituted membrane phospholipids
in Sertoli cell polarity and blood-testis barrier, and the gap
junction network between granulosa cells of ovarian follicles. The
fads2 -/- mouse is an auxotrophic mutant. It is anticipated that FADS2
will become a major focus in membrane, haemostasis, inflammation and
atherosclerosis research.
PMID: 19172737
- those idiots cannot even think of the Mead acid being synthesized by
the same desaturase enzyme, let alone to bother to include it as a
control in their experiments with the mutant. Countless experimental
animals are being slaughtered on daily basis in the scientific plays
like this ...
Taka |
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