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Re: Magnesium and sore/tender breasts?

Posted by honeybee on May 31, 2006, at 15:04:52

In reply to Re: Magnesium and sore/tender breasts? » honeybee, posted by Larry Hoover on May 31, 2006, at 12:27:32

It's definitely a mystery.

But, Larry, maybe you can suss out a little more information from this article than I?

http://www.pdrhealth.com/drug_info/nmdrugprofiles/nutsupdrugs/eve_0291.shtml

Under "Mechanism of Action" it reads:

The possible anti-inflammatory and anti-aggregatory actions of EPO may be accounted for by examining the role of GLA in eicosanoid biochemistry. GLA is metabolized to the 20-carbon polyunsaturated fatty acid dihomo-gamma-linolenic acid (DGLA; 20: 3n-6), which is a precursor to the 1-series prostaglandins, such as prostaglandin E1 (PGE1). The action of PGE1 on inflammatory cells (e.g., polymorphonuclear leukocytes or PMNs) is mostly inhibitory. PGE1 increases intracellular cyclic AMP (cAMP). This increase reduces the release of lysosomal enzymes, PMN chemotaxis and the margination and adherence of PMNs in the blood vessels. PGE1 is also thought to inhibit lymphocyte function.

PGE1, in addition to its role in suppressing the inflammatory process, inhibits platelet aggregation and has vasodilatory activity.

GLA, via its metabolite DGLA, has an inhibitory effect on leukotriene (LT) synthesis. Leukotriene B4 (LTB4) is an inflammatory mediator. DGLA is metabolized to 15-hydroxyl DGLA, which blocks the conversion of arachidonic acid to LTs, such as LTB4.

In summary, GLA may suppress inflammation through its metabolism to DGLA, which, in turn, can competitively inhibit the pro-inflammatory 2-series prostaglandins and 4-series leukotrienes. The incorporation of GLA and its metabolites in cell membranes may also play a role in the possible anti-inflammatory, antithrombotic, anti-atherogenic and antiproliferative actions of EPO.

It's still greek to me...(and I don't speak Greek.)


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URL: http://www.dr-bob.org/babble/alter/20060428/msgs/651084.html