Hans,
can we open this new thread gathering scientific information about the Mead acid? I think it is important to demonstrate that the Mead acid can substitute for all the AA/EPA/GLA functions the "experts" feel to be essential for healthy life. It's amazing to see that Mead acid is the main component of membranes in young, growing and healthy tissues ... I will start with some abstracts:
Lipids. 1995 Oct;30(10):949-53.
Differences in fatty acid composition of immature and mature articular cartilage in humans and sheep.
Cleland KA, James MJ, Neumann MA, Gibson RA, Cleland LG.
Rheumatology Unit, Royal Adelaide Hospital, Australia.
Chondrocytes are imbedded in an avascular, highly charged extracellular matrix which could form a barrier to the transfer of dietary essential fatty acids (EFA) to chondrocytes. A study was designed to assess the composition of immature and mature joint cartilage with respect to essential and nonessential fatty acids relevant to EFA deficiency. Cartilage and muscle samples were obtained from human fetus, infant and adult cadavers, and from fetal and mature sheep. Lipid extracts were prepared and the fatty acid composition determined. In human and sheep joint cartilage, linoleic acid (LA; 18:2n-6) content was lower, and n-9 eicosatrienoic acid (ETrA; 20:3n-9) and arachidonic acid (AA; 20:4n-6) were higher in fetuses compared to mature subjects. An intermediate pattern was seen in infant cartilage. n-3 Fatty acids tended to be higher in fetal than in mature cartilage in humans and in sheep. In human muscle (and in other noncartilaginous comparison tissues), similar differences between fetuses and adults were seen in LA and AA, but not in ETrA. In fetal sheep muscle, very low LA, reduced AA and raised ETrA levels compared to mature sheep muscle were seen. However, although the pattern is characteristic of EFA deficiency, the abundance of n-6 EFA in liver and spleen of human fetuses and of n-3 EFA in liver and spleen of fetal sheep suggests that placental transfer of EFA is not likely to be limiting. During fetal development, the metabolism of fatty acids is distinctive and differs between the species. ETrA appears to be a readily measurable component of some tissues at certain stages of development when its presence in tissues does not indicate EFA deficiency.
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.
J Biol Chem. 1983 Nov 10;258(21):12797-800.
Products derived from 5,8,11-eicosatrienoic acid by the 5-lipoxygenase-leukotriene pathway.
Jakschik BA, Morrison AR, Sprecher H.
Analysis of products derived from 5,8,11-eicosatrienoic acid via the 5-lipoxygenase-leukotriene pathway showed that this fatty acid is readily converted to leukotriene (LT)A3. When 10,000 X g supernatant from rat basophilic leukemia cell homogenates was incubated with 30 microM fatty acid, 5,8,11-eicosatrienoic acid produced 6.2 +/- 1.1 nmol of LTA3 and arachidonic acid 15.5 +/- 1.9 nmol of LTA4 (n = 4). However, only insignificant amounts of LTB3 were formed (0.15 +/- 0.04 nmol of LTB3 and 4.2 +/- 0.4 nmol of LTB4, n = 4). These data indicate that the LTA-hydrolase requires not only the three double bonds of the triene but also the double bond at C-14 to efficiently convert LTA to LTB. These findings have significant implications for essential fatty acid deficiency.
J Biol Chem. 1984 Oct 10;259(19):11784-9.
Leukotriene B formation by neutrophils from essential fatty acid-deficient rats.
Stenson WF, Prescott SM, Sprecher H.
Analysis of neutrophil phospholipids from rats fed an essential fatty acid-deficient diet revealed a 33% reduction in arachidonate and a 90% reduction in linoleate compared to neutrophil phospholipids of rats fed a normal diet. The neutrophil phospholipids from rats fed the essential fatty acid-deficient diet also contained significant amounts of 5,8,11-eicosatrienoate, a fatty acid not found in the neutrophils of rats fed a normal diet. Analysis of the production of leukotrienes of the B series by ionophore-stimulated neutrophils from rats fed an essential fatty acid-deficient diet revealed a 87% reduction in leukotriene B4 compared to neutrophils from rats fed a normal diet even though the arachidonate content was reduced by only 34%. Essential fatty acid-deficient neutrophils converted endogenous 5,8,11-eicosatrienoic acid to leukotriene A3 and its nonenzymatic degradation products, but little or no leukotriene B3 was formed. Neutrophils from rats fed a normal diet incubated with ionophore and exogenous 5,8,11-eicosatrienoate also produced leukotriene A3 and its nonenzymatic degradation products but little or no leukotriene B3. Exogenous 5,8,11-eicosatrienoate incubated with ionophore-stimulated normal neutrophils caused a dose-dependent inhibition of leukotriene A hydrolase resulting in diminished production of leukotriene B4 from endogenous arachidonate. Assays of leukotriene A hydrolase in the 10,000 X g supernatant fraction of a homogenate of RBL-1 cells revealed that a lipoxygenase metabolite of 5,8,11-eicosatrienoate rather than 5,8,11-eicosatrienoate itself is the inhibitor of leukotriene A hydrolase. Thus the finding that leukotriene B4 production by neutrophils from essential fatty acid-deficient rats is diminished out of proportion to the decrease in arachidonate content appears to be due to inhibition of leukotriene A hydrolase by a lipoxygenase metabolite. |
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