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Submited By: Lia on 07/05/2008
Evening primrose oil was one of the first nutritional / botanical supplements to gain popularity in the renaissance of ‘alternative medicine’. The popularity of evening primrose oil supplements is such that in 1993 a survey of complementary medicine use in Australia showed that over 12% of all women supplemented with Evening Primrose! The whole Evening Primrose plant has been used for the management of many conditions, including gastrointestinal disorders, asthmatic coughs, neuralgia and whooping cough. These numerous indications gave rise to the plant being commonly referred to as the "King's Cure All".
As a source of pre-formed gamma linolenic acid ("GLA"), evening primrose oil may be of use in a number of conditions, especially those with an inflammatory component. Evening Primrose is commonly used in women’s health care for treating premenstrual syndrome, mastalgia endometriosis and atopic eczema. Evening primrose is also used in rheumatoid arthritis, multiple sclerosis, and Sjogren’s syndrome, as well as certain psychiatric conditions, such as hyperactivity, dementia and schizophrenia. Regardless of the reason for taking evening primrose oil, it needs to be taken for a prolonged period of time (over 6 months) for best results.
* Essential Fatty Acids *
To understand the suggested pharmacology of evening primrose oil, it is necessary to review some basic points regarding essential fatty acid (EFA) biochemistry and nomenclature. By definition, an essential fatty acid is one that the body cannot make. There are two basic types, omega 3 (derived from a-linolenic acid) and omega 6 (derived from linoleic acid). These essential fatty acids are polyunsaturated (containing more than one double bond). The naming of a particular fatty acid is made by determining the position of the first double bond from the methyl end of the carbon-carbon backbone of the molecule. For example, an omega 3 fatty acid contains a double bond between the third and fourth carbon atom. The essential fatty acids have a 'cis' rather than a 'trans' configuration and the omega 3 and omega 6 series are not interchangeable.
Both alpha-linolenic and linoleic acid can be modified via desaturation or elongation reactions. While neither alpha-linolenic acid nor linoleic acid have any direct biological effect, their metabolites have pronounced physiological properties. The enzymatic mechanism by which these changes occur is very similar, if not identical, in both the omega 3 and omega 6 series. The physiological action of EFAs occurs in one of two primary ways. EFAs play a role in the physical properties of cell membranes, influencing their flexibility and fluidity and thus they impact membrane based receptors and systems. EFAs also act as precursors of biologically active eicasonoids such as prostaglandins and leukotrienes.
In the omega 6 series, cis-linoleic acid (LA) is converted to gamma-linolenic acid (GLA), which in turn is converted to dihomogamma-linolenic acid (DGLA). The rate-limiting step for this process is the desaturation of LA to GLA by the enzyme delta-6 desaturase. The DGLA can then be metabolized further to form arachadonic acid (AA) by delta-5 desaturase. DGLA can also be acted upon by cyclo-oxygenase to form prostaglandin E1 (PGE1). PGE1 is generally regarded as being beneficial, inhibiting inflammation and platelet aggregation, decreasing blood pressure and regulating the immune system. Conversely, arachidonic acid gives rise to harmful pro-inflammatory mediators. While it may be assumed that any increase in GLA would lead to a subsequent increase in both the anti-inflammatory and inflammatory moieties, this appears not to be the case. Administration of large amounts of GLA increases DGLA levels but not AA. It is thought that the beneficial metabolites of DGLA (including PGE!
1) play a role in limiting the release of arachidonic acid from its phospholipid stores. Also, while the conversion of GLA to DGLA is rapid, the activity of delta-5 desaturase is quite slow.
Since the body can manufacture GLA, theoretically it should not be considered an essential fatty acid. In practice this may not be the case due to the inefficiency of the rate limiting enzyme mentioned above, delta-6 desaturase. This enzyme system appears to be compromised in many situations, including aging; diabetes; excessive consumption of alcohol; viral infections; and atopic eczema. A deficiency in certain nutritional cofactors (e.g. zinc, pyridoxine, and magnesium) can also lead to a decreased activity of this enzyme system. The existence of a decreased rate of delta-6 desaturation in atopic individuals is not universally accepted.
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