Do a pubmed.com search for arachidonic toxic...
- From: montygraham <monty1945@xxxxxxxxx>
- Date: Fri, 19 Jun 2009 23:38:34 -0700 (PDT)
....and you find some very interesting abstracts, such as:
J Neurochem. 2007 May;101(3):577-99. Epub 2007 Jan 25.
Modulation of inflammation in brain: a matter of fat.
Farooqui AA, Horrocks LA, Farooqui T.
Department of Molecular and Cellular Biochemistry, The Ohio State
University, Columbus, Ohio 43210, USA.
Neuroinflammation is a host defense mechanism associated with
neutralization of an insult and restoration of normal structure and
function of brain. Neuroinflammation is a hallmark of all major CNS
diseases. The main mediators of neuroinflammation are microglial
cells. These cells are activated during a CNS injury. Microglial cells
initiate a rapid response that involves cell migration, proliferation,
release of cytokines/chemokines and trophic and/or toxic effects.
Cytokines/chemokines stimulate phospholipases A2 and cyclooxygenases.
This results in breakdown of membrane glycerophospholipids with the
release of arachidonic acid (AA) and docosahexaenoic acid (DHA).
Oxidation of AA produces pro-inflammatory prostaglandins,
leukotrienes, and thromboxanes. One of the lyso-glycerophospholipids,
the other products of reactions catalyzed by phospholipase A2, is used
for the synthesis of pro-inflammatory platelet-activating factor.
These pro-inflammatory mediators intensify neuroinflammation. Lipoxin,
an oxidized product of AA through 5-lipoxygenase, is involved in the
resolution of inflammation and is anti-inflammatory. Docosahexaenoic
acid is metabolized to resolvins and neuroprotectins. These lipid
mediators inhibit the generation of prostaglandins, leukotrienes, and
thromboxanes. Levels of prostaglandins, leukotrienes, and thromboxanes
are markedly increased in acute neural trauma and neurodegenerative
diseases. Docosahexaenoic acid and its lipid mediators prevent
neuroinflammation by inhibiting transcription factor NFkappaB,
preventing cytokine secretion, blocking the synthesis of
prostaglandins, leukotrienes, and thromboxanes, and modulating
leukocyte trafficking. Depending on its timing and magnitude in brain
tissue, inflammation serves multiple purposes. It is involved in the
protection of uninjured neurons and removal of degenerating neuronal
debris and also in assisting repair and recovery processes. The
dietary ratio of AA to DHA may affect neurodegeneration associated
with acute neural trauma and neurodegenerative diseases. The dietary
intake of docosahexaenoic acid offers the possibility of counter-
balancing the harmful effects of high levels of AA-derived pro-
inflammatory lipid mediators.
MY NOTE: As usual, the authors don't even consider the possibility
that all the problems they mention can be totally avoided by having
the natural Mead acid in your cells instead of any omega 3s or 6s, and
so they don't have a control, which is a basic tenet of the scientific
method. Thus, when you "close your mind," you can end up doing anti-
scientific things because you do experiments without proper controls.
In this case, the conclusion many "experts" draw is that people should
supplement with omega 3s, but most of them are probably unaware of the
dangers of omega 3s, as well as the Mead acid idea. For example:
Crit Rev Food Sci Nutr. 2008 Feb;48(2):119-36.
Toxic oxygenated alpha,beta-unsaturated aldehydes and their study in
foods: a review.
Guillén MD, Goicoechea E.
Tecnología de Alimentos, Facultad de Farmacia, UPV, Paseo de la
Universidad N 7, Vitoria, Spain. knpgulod@xxxxxxxxx
The oxidation of lipids containing polyunsaturated omega-3 or omega-6
acyl groups, such as docosahexenoic, eicosapentenoic, linolenic,
arachidonic, or linoleic groups, and of the corresponding fatty acids,
generates among other compounds alpha,beta -unsaturated aldehydes
supporting different functional groups containing oxygen, which can be
named oxygenated alpha,beta -unsaturated aldehydes (OalphabetaUAs).
These compounds can be produced in cells and tissues of living
organisms or in foods during processing or storage, and from these
latter can be absorbed through the diet. In the last few years,
OalphabetaUAs are receiving a great deal of attention because they are
being considered as possible causal agents of numerous diseases, such
as chronic inflammation, neurodegenerative diseases, adult respiratory
distress syndrome, atherogenesis, diabetes, and different types of
cancer. This review deals with the nature of the different kinds of
OalphabetaUAs detected until now, their reactivity and consequent
biological activity; the several pathways proposed for their
formation; the current knowledge about the influence of both oxidative
conditions and lipids nature in the rate of formation and yield of
each kind of OalphabetaUAs in edible oils; the methods described until
now to determine the presence in foods of some of these compounds,
such as 4-hydroxy-trans-2-nonenal, 4-hydroxy-trans-2-octenal, 4-
hydroxy-trans-2-hexenal and 4-oxo-trans-2-hexenal; and finally, the
levels found of some of them in several foods.
.
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