I think you've got some valid points Alf, but I'd like to see you cite some
studies, instead of acting like you know "the truth" and thereby don't have
to conform to scientific convention. About this part of one of your posts:
"The key of decreasing omega-6/omega-3 ratio is that it will involve an increased inhibition of the
delta-5 desaturase, that will in fact increase the 20:3(DHGLA) to 20:4(arachidonate) ratio and thus
increase the amount of PGH1 and PGH3 on behalf of PGH2, and thus less PGE2/PGF2alfa,PGI2,TXA2 etc.
And increase PGI3 and ineffective TXA's, plus PGE1 and PGE3 which are working as antidotes on PGE2.
There is a ying/yang balance out there to say it that way. Nick seems to forget that, Free radicals
are mostly only of concern when you are totally devoid of copper, manganese, selenium and Vit E and
vit C in diet. But the higher omega-6 to omega-3 ratio, the demands on these ingredients in diet are
rising, in some skyrocking manner, Mead acid do no good at all. Except for being inert, almost. When
you have a wound, you will have it for years if cell membranes only contain Mead acid. Because no
signals are formed to signal need for repair."
Now there have been investigations into people who are EFAD, and I've never seen this delayed
healing process you mention described by any of them. I'll cite some sources that appear to
contradict this point of yours, and now it's your turn to cite some source - or shut up!
"Adkisson, H.D., Tranik,T.M., & Wuthier,R.E. Relationship of cartilage Mead acid levels to aging and
development of osteoarthritis. The authors studies the relationship of cartilage mead acid levels to
aging and development of osteoarthritis. They looked at the fatty acid status of weight-bearing and
non-weight bearing cartilage from autopsy specimens, or from surgical procedures, in various ages
and disease states. Young cartilage is characterised by the presence of high levels of 20:9 w-9,
Mead acid, indicating a relative deficiency of EFA. Skeletal muscle from the same subjects showed
normal EFA levels, and no Mead acid. Age decreases the Mead acid level and increases the EFA level,
with weight-bearing cartilage having more EFA and less Mead acid than costal tissues. Cartilage from
osteoarthritis affected joints showed even lower Mead acid levels and even higher w-6 EFA levels,
leading the authors to speculate that accumulation of w-6 EFAs in cartilage might predispose towards
the development of OA, and that the presence of Mead acid might somehow be protective. They also
speculate that weight-bearing cartilage might be better vascularised than costal tissue. Poster
Presentation at the Third International Conference on Essential Fatty Acids and Eicosanoids,
Adelaide, Australia March 1 1992
J. Biol. Chem., Vol. 261, Issue 15, 6719-6724, May, 1986"
"J Exp Med. 1993 Dec 1;178(6):2261-5. Effect of dietary supplementation with n-9 eicosatrienoic acid
on leukotriene B4 synthesis in rats: a novel approach to inhibition of eicosanoid synthesis.
James MJ, Gibson RA, Neumann MA, Cleland LG.
Rheumatology Unit, Royal Adelaide Hospital, Adelaide, South Australia.
Studies were undertaken to assess the biochemical effects of dietary supplementation with n-9
eicosatrienoic acid (ETrA), an arachidonic acid analogue that is normally present in cell membranes
at very low levels but is raised in the presence of essential fatty acid deficiency (EFAD). The
incorporation of dietary ETrA into rat neutrophils and its effect on A23187-stimulated 5-
lipoxygenase metabolism in these cells was examined; in addition, the effect of ETrA was compared
with that of another arachidonic acid analogue, eicosapentaenoic acid (EPA), which is known to
accumulate in cell membranes and inhibit synthesis of leukotriene B4 (LTB4) a product of the 5-
lipoxygenase metabolic pathway. Rats were fed a defined diet that was sufficient in essential fatty
acids and that contained EPA or ETrA (0.014% of energy) or no added fatty acid, for 3 wk. In the
cells from ETrA-fed rats, LTB4 synthesis was inhibited relative to control values, but synthesis of
the other products of 5-lipoxygenase metabolism, 5-hydroxyeicosatetraenoic acid (5-HETE) and the all-
trans isomers of LTB4, were not inhibited. This pattern indicates inhibition of LTA hydrolase in ETrA-
fed rats. In EPA-fed rats, there was inhibition of LTB4 and the all-trans isomers of LTB4, but there
was no inhibition of 5-HETE. This pattern indicates inhibition of LTA synthase in EPA-fed rats. The
results establish that dietary ETrA effectively inhibits synthesis of the inflammatory mediator,
LTB4, and suggest that ETrA may confer antiinflammatory benefits similar to those observed with EFAD
or dietary fish oil (which contains EPA). Because ETrA is substantially less unsaturated than EPA,
it can be expected to have greater chemical stability, which could be an important practical
advantage when used as a dietary constituent or supplement. "
"FASEB J. 1991 Mar 1;5(3):344-53. Unique fatty acid composition of normal cartilage: discovery of
high levels of n-9 eicosatrienoic acid and low levels of n-6 polyunsaturated fatty acids.
Adkisson HD 4th, Risener FS Jr, Zarrinkar PP, Walla MD, Christie WW, Wuthier RE.
Department of Chemistry, University of South Carolina, Columbia 29208.
We report here the finding that normal, young cartilages, in distinction from all other tissues
examined, have unusually high levels of n-9 eicosatrienoic (20:3 cis-delta 5,8,11) acid and low
levels of n-6 polyunsaturated fatty acids (n-6 PUFA). This pattern is identical to that found in
tissues of animals subjected to prolonged depletion of nutritionally essential n-6 polyunsaturated
fatty acids (EFA). This apparent deficiency is consistently observed in cartilage of all species so
far studied (young chicken, fetal calf, newborn pig, rabbit, and human), even though levels of n-6
PUFA in blood and all other tissues is normal. The n-9
20:3 acid is particularly abundant in phosphatidylethanolamine, phosphatidylinositol, and the free
fatty acid fractions from the young cartilage. Several factors appear to contribute to the
reduction in n-6 PUFA and the appearance of high levels of the n-9 20:3 acid in cartilage: 1)
limited access to nutritional sources of EFA due to the impermeability and avascularity of
cartilage, 2) rapid metabolism of n-6 PUFA to prostanoids by chondrocytes, and 3) a unique fatty
acid metabolism by cartilage. Evidence is presented that each of these factors contributes.
Previously, EFA deficiency has been shown to greatly suppress the inflammatory response of
leukocytes and rejection of tissues transplanted into allogeneic recipients. Because eicosanoids,
which are derived from EFA, have been implicated in the inflammatory responses associated with
arthritic disease, reduction of n-6 PUFA and accumulation of the n-9 20:3 acid in cartilage may
be important for maintaining normal cartilage structure.
PMID: 2001795 [PubMed - indexed for MEDLINE]"
"Lipids. 1996 Aug;31(8):829-37. Effect of dietary n-9 eicosatrienoic acid on the fatty acid
composition of plasma lipid fractions and tissue phospholipids.
Cleland LG, Neumann MA, Gibson RA, Hamazaki T, Akimoto K, James MJ.
Rheumatology Unit, Royal Adelaide Hospital, Australia. n-9 Eicosatrienoic acid (ETrA), also known as
Mead acid, is a minor fatty acid in essential fatty acid (EFA)-sufficient healthy subjects but is
found at increased levels in EFA deficiency. This study examined the influence of dietary ETrA from
a biological source on plasma and tissue ETrA. A synthetic fat-free diet was prepared to which was
added Mut 48 oil which contains 19% ETrA (wt%) as well as other n-9 fatty acids. Blends of vegetable
oils were used to achieve overall diets with 5% fat (wt%) and varying amounts of ETrA at two
different dietary levels of linoleic acid (LA), approximately 4.4 and 19% of total fatty acids.
These diets were fed to 5-week-old Dark Agouti rats for four weeks. Plasma lipid fractions and
liver, spleen, and peritoneal exudate (PE) cells were analyzed for fatty acid composition. ETrA was
present at up to 20% total fatty acids in plasma triglyceride, cholesterol ester, and phospholipid
fractions. ETrA also accumulated to substantial levels in phospholipids of liver and spleen (up to
15% of total fatty acids) and PE cells (up to 11%). ETrA was found in plasma and tissue
phospholipids in proportion to the amount of ETrA present in the diet. The incorporation was reduced
in diets with higher LA content compared to diets containing similar amounts of ETrA but lower LA.
All rats remained apparently healthy, and histological survey of major organs revealed no
abnormality. While the long-term implications for health of ingestion of diets rich in ETrA remain
to be established, rats appear to tolerate high levels of dietary ETrA without adverse effects.
Dietary enrichment with ETrA warrants further investigation for possible beneficial effects in
models of inflammation and autoimmunity, as well as in other conditions in which mediators derived
from n-6 fatty acids can affect homeostasis adversely.
PMID: 8869885 [PubMed - indexed for MEDLINE]"