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Old 10-07-2008, 05:36 PM
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fmichael fmichael is offline
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Join Date: Sep 2006
Location: California
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fmichael fmichael is offline
Senior Member
fmichael's Avatar
 
Join Date: Sep 2006
Location: California
Posts: 1,239
15 yr Member
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Sorry to get in late here, but I was advised some time ago by a prof in the Dept. of Neurobiology at UCLA that the best way to control inflamation - and specifically sympathetic tone as modulated by the insular cortex in the brain - was through a diet rich in Omega-3 fatty acids. He said that approx. 2,400 mg./day should be about right. To that end, please see the following abstract:

Modulation of inflammatory cytokines by omega-3 Fatty acids. Kang JX, Weylandt KH. Subcell Biochem. 2008; 49: 133-43.

Department of Medicine, Massachusetts General Hospital, Harvard Medical School, 02114, Boston, MA, USA.

Many human diseases have been linked to inflammation, which is mediated by a number of chemical molecules including lipid mediators and cytokines. Polyunsaturated fatty acids (omega-6 and omega-3 fatty acids) are the precursors of the lipid mediators and play an important role in regulation of inflammation. Generally, omega-6 fatty acids (e.g. arachidonic acid) promote inflammation whereas omega-3 fatty acids (e.g. eicosapentaenoic acid and docosahexaenoic acid) have anti-inflammatory properties. Omega-3 fatty acids dampen inflammation through multiple pathways. On the one hand, omega-3 fatty acids inhibit the formation of omega-6 fatty acids-derived pro-inflammatory eicosanoids (e.g. PGE(2) and LTB(4)), and on the other hand these fatty acids can form several potent anti-inflammatory lipid mediators (e.g. resolvins and protectins). These together directly or indirectly suppress the activity of nuclear transcription factors, such as NFkappaB, and reduce the production of pro-inflammatory enzymes and cytokines, including COX-2, tumor necrosis factor (TNF)-alpha, and interleukin (IL)-1beta. This chapter focuses on the evidence from recent studies using new experimental models.
What's also of note is what may increase inflammatory processes. While we all know about stress, there's been recent work done that shows the mechanism of "Association of catastrophizing with interleukin-6 responses to acute pain," Robert R. Edwards at al, Pain epub 2008.07.24, a copy of which is attached for anyone who's interested. It's a very interesting article that can probably be read on a number of levels, but it basically demonstrates that “catastrophizing” produces inflammatory cytokines in and of itself.

Ironically, it's also been established, at least in the context of arthritis that SSRI antidepressants may actually increase the inflammatory processes. See, "Alteration of central serotonin modifies onset and severity of adjuvant-induced arthritis in the rat," M.S. Harbuz et al, British Journal of Rheumatology, 1998 Oct; 37(10):1077-83, a copy of which is also attached. For what it's worth . . . (I know they drove my RSD induced spasms to insane levels.)

Mike
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