Regulatory Functions Influence of Nutrition

Many studies have shown that fatty acid patterns can be affected by ingestion of particular fatty acids (A). This opens the possibility of influencing cell membrane fluidity and associated membrane protein functions as well as eicosanoid synthesis through dietary measures.

Many experiments are based on the administration of higher level homologues of the essential fatty acids, lino-leic and a-linolenic acid. The underlying assumption is that in certain diseases the first enzyme of the enzyme pathway, 5-6-desaturase, does not work properly. Since activity of this enzyme cannot be measured directly, indirect proof—higher substrate concentrations compared to lower product concentrations—is used. Since 5-6-desaturase is the rate-limiting enzyme, marginal activity levels could have wide-ranging consequences.

Based on this, the product of 5-6-desat-urase in the n-6 pathway, y-linolenic acid, is supplemented in the form of specific plant oils. When high levels of y-linolenic acid are supplied, amounts of mainly the next intermediary, dihomo-y-linolenic acid, are elevated predominantly in membranes. Di-homo-y-linolenic acid can be converted to arachidonic acid, but it is also the direct precursor of series 1 eicosanoids. Since eicosanoids have effects in nano-and picogram ranges, and the different series are often antagonistic, minor changes in their balance are often sufficient to achieve clinically relevant effects.

Restriction of arachidonic acid intake through purely vegetarian nutrition, which has been practiced for a long time, is founded on a similar basis. It lowers arachidonic acid metabolite levels, especially the series 4 eicosanoids. Leucotriene B4, one of the eicosanoids of this series, has pronounced chemo-tactic effects, stimulating the migration of eosinophile leukocytes, and thereby enhancing inflammation. Both therapeutic approaches, y-linolenic acid supplementation for neurodermatitis, as well as reduction of arachidonic acid intake for rheumatic illnesses, are subject to controversial discussion.

Oral administration of higher-level homologues of the n-3-fatty acid pathway in the form of fish oils aims at similar goals. The example of chemotactic effects of leukotrienes can be used to demonstrate their role in inflammation: eicosapentaenoic acid (n-3) competes with arachidonic acid (n-6) for the enzyme lipoxygenase. The chemotactic effect of LTB5 (which forms preferentially at high n-3 levels) compared to LTB4 (which forms preferentially at higher arachidonic acid levels) is much lower and hence tends to inhibit inflammation.

N-3 fatty acids have also become known for another effect: inhibition of thrombocyte aggregation. It is assumed that native Greenland Eskimos' propensity to bleed, combined with their low incidence of coronary artery disease (CAD) is due to their high fish intake. Large amounts of n-3 fatty acids are found in wild ocean fish. Farm-raised ocean fish and freshwater fish have a different fatty acid spectrum than wild ocean fish. Oral fish oil supplementation for CAD prevention, however, is still controversial.

Regulatory Functions III

- A. Nutritional Modification of Fatty Acid Composition -

n-6 Fatty acids

Intake of

Evening primrose oil borage oil, etc.

Reduction of Arachidonic acid intake Meat, eggs j n-3 Fatty acids

Intake of

Fish oils, flax seed oil

Evening primrose oil borage oil, etc.

Reduction of Arachidonic acid intake Meat, eggs j

Fish oils, flax seed oil

y-Linolenic acid f Dihomo-y-linolenic acid f Fluidity f ?

Series 1 f n-3 Fatty acids f Fluidity f

Series 2 j Series 4 j

Inflammation j ? Thrombocyte aggregation j ?

Inflammation j ?

Neurodermatitis

Rheumatic disease

Series 3 f Series 5 f n-6 Eicosanoids j

Thrombocyte aggregation j ?

Inflammation j ?

Blood pressure j ?

Prevention (CVD)

Rheumatic disease

Dietary measures

Membrane structure

Eicosanoid synthesis

Patho-physiological effects

Suggested applications

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