Herbal Use/Indication
An infusion of the whole plant is thought to have a sedative and astringent properties, and has traditionally been used for asthmatic coughs, gastrointestinal disorders, whooping cough, and as a sedative painkiller. Poultices were reputed to ease bruises and to speed wound-healing.
(48)
Evening Primrose oil has been used for premenstrual syndrome, psoriasis, multiple sclerosis, hypercholesterolaemia, rheumatoid arthritis, Reynaurd's phenomenon, Sjorgren's syndrom, post-viral fatigue syndrome, asthma, and diabetic neuropathy. (48)(49)(50)(51)
Evening Primrose oil has been used for premenstrual syndrome, psoriasis, multiple sclerosis, hypercholesterolaemia, rheumatoid arthritis, Reynaurd's phenomenon, Sjorgren's syndrom, post-viral fatigue syndrome, asthma, and diabetic neuropathy. (48)(49)(50)(51)
Pharmacological Action
The seed oil of evening primrose contains the EFAs linoleic acid and gamma-linolenic acid (GLA). Both are prostaglandin precursors. GLA is though to increase the ratio of non-inflammatory compounds.
(1)
GLA and its metabolite dihomogamma-linolenic acid (DGLA) are precursors of both of the inflammatory prostaglandins E2 (PGE2) series via arachadonic acid (AA), and the less inflammatory prostaglandin E1 (PGE1) series. (1)
PGE1 acts as an anti-inflammatory, immunoregulatory, vasodilator, inhibits platelet aggregation and cholesterol bio-synthesis, promotes hypo-tension, and elevates cyclic AMP (inhibits phospholipase A2). (49)(50)(51)
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GLA and its metabolite dihomogamma-linolenic acid (DGLA) are precursors of both of the inflammatory prostaglandins E2 (PGE2) series via arachadonic acid (AA), and the less inflammatory prostaglandin E1 (PGE1) series. (1)
PGE1 acts as an anti-inflammatory, immunoregulatory, vasodilator, inhibits platelet aggregation and cholesterol bio-synthesis, promotes hypo-tension, and elevates cyclic AMP (inhibits phospholipase A2). (49)(50)(51)
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GLA is thought to increase the DGLA:AA ratio. DGLA inhibits the conversion of arachidonic acid to inflammatory lipoxygenase metabolites such as leukotrienes.
(1)
PGE1 inhibits the enzyme phospholipase A2, which is responsible for removing AA from the phospholipid membrane stores. DGLA desaturation to AA is a rate-limiting step in humans and proceeds slowly. (51)
The body metabolizes linolenic acid (LA) to gamma-linolenic acid (GLA). This conversion is reduced in aging, diabetes, cardiovascular disorders, and high cholesterol intake, high alcohol intake, viral infections, cancer, nutritional deficits, atopic eczema, and PMS. (49)(50)(51)
Direct dietary supplementation of GLA bypasses this slow-step, converting LA to GLA, and increases the ratio of DGLA:AA.
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PGE1 inhibits the enzyme phospholipase A2, which is responsible for removing AA from the phospholipid membrane stores. DGLA desaturation to AA is a rate-limiting step in humans and proceeds slowly. (51)
The body metabolizes linolenic acid (LA) to gamma-linolenic acid (GLA). This conversion is reduced in aging, diabetes, cardiovascular disorders, and high cholesterol intake, high alcohol intake, viral infections, cancer, nutritional deficits, atopic eczema, and PMS. (49)(50)(51)
Direct dietary supplementation of GLA bypasses this slow-step, converting LA to GLA, and increases the ratio of DGLA:AA.