Posted by Larry Hoover on April 22, 2003, at 9:19:45
In reply to Re: FO vs. E-EPA Ron and noa, posted by noa on April 22, 2003, at 7:37:26
> Thanks, Larry, for those insights.
>
> I guess I am also wary of drawing too many conclusions from the research as it is still early in the research process--few studies, still small, etc.
>
> But I enjoy your help in interpreting information.
>
> I'm still "digesting" the info on the synergy between the GLA and EPA/DHA etc. It's getting complicated! But I'll reread your posts and "absorb" it in time.
>
> Thanks. Hope you are continuing to feel healthier!I'm feeling better, thanks. Except, the last thing I want to do is overwhelm people with information. That serves no purpose, ya know?
Can I help you with anything?
Lar
P.S. Here's an abstract about the GLA/lipoic acid synergy:
Diabetologia 1998 Apr;41(4):390-9
Effects of alpha-lipoic acid on neurovascular function in diabetic rats: interaction with essential fatty acids.Cameron NE, Cotter MA, Horrobin DH, Tritschler HJ.
Department of Biomedical Sciences, University of Aberdeen, Scotland, UK.
Elevated oxidative stress and impaired n-6 essential fatty acid metabolism contribute to defective nerve conduction velocity (NCV) and perfusion in diabetic rats, which may be corrected by free radical scavenger and gamma-linolenic acid (GLA) treatments. Alpha-lipoic acid (LPA) has antioxidant actions and both LPA racemate (racLPA) and GLA treatments produced benefits in clinical neuropathy trials. The aims were to study LPA action on neurovascular function in diabetic rats and to investigate potential interactions for co-treatment with GLA and other essential fatty acids. After 6 weeks of diabetes, 2 weeks of racLPA treatment corrected 20% sciatic motor and 14% saphenous sensory NCV deficits. The ED50 for motor NCV restoration was approximately 38 mg kg(-1) day(-1). racLPA also corrected a 49% diabetic deficit in sciatic endoneurial blood flow. R and S-LPA enantiomers were equipotent in correcting NCV and blood flow deficits. Treatment of diabetic rats with low doses (20 mg kg(-1) day(-1)) of racLPA and GLA, while having modest effects on their own, showed evidence of marked synergistic action in joint treatment, completely correcting motor NCV and blood flow deficits. This was also noted for the novel compound, SOC0150, which contains equimolar proportions of LPA and GLA (ED50 9.3 mg kg(-1) day(-1), containing 3.5 mg LPA). NCV effects also showed marked synergism when racLPA:GLA ratios were varied over a 1:3-3:1 range. In contrast, a compound containing LPA and the n-3 component, docosahexaenoic acid, showed similar activity to LPA alone. Thus, LPA-GLA interactions yield drug combinations and compounds with an order of magnitude increase in efficacy against experimental diabetic neuropathy and are worthy of consideration for clinical trials.
And here's one of the easier to understand ones that demonstrate that GLA suppresses the artery-damaging pathology in atherosclerosis:Adv Exp Med Biol 1999;469:485-91
Modulation of atherogenesis by dietary gamma-linolenic acid.
Fan YY, Ramos KS, Chapkin RS.
Faculty of Nutrition, Texas A&M University, College Station 77843, USA.
Data from our in vitro studies indicate that macrophages isolated from mice fed GLA-enriched diets inhibit vascular SMC proliferation via a PGE1-cAMP dependent mechanism. Since SMC proliferation is one of the main events implicated in the pathogenesis of atherosclerosis (Ross, 1993), this anti-proliferative effect observed by dietary GLA is noteworthy. In vivo studies have established that dietary GLA is capable of retarding the atherosclerotic lesion formation in ApoE knock out mice, an animal model that develops atherosclerosis similar to humans (Reddick, 1994). We propose that dietary GLA has the potential to inhibit SMC proliferation leading to retardation of atherosclerotic lesion formation, and therefore favorable modulation of the atherogenic process.
poster:Larry Hoover
thread:216908
URL: http://www.dr-bob.org/babble/20030417/msgs/221419.html