Herbfacts

Evening Primrose Oil

Latin name; Oenothera biennis

Other names: King’s cure-all

About Evening Primrose Oil

Evening primrose oil (EPO), is obtained by cold expression or solvent extraction from the seeds of the evening primrose plant (1). Native to North and South America and now widespread throughout Europe and parts of Asia, this biennial plant is also known by the names tree primrose, sun cups, sundrops, king’s cure-all, fever plant, evening star, and night willow-herb.

Native Americans valued its mucilaginous stem and leaf juices as topical remedies to soothe cutaneous inflammation, whereas poultices of the plant were used to treat bruises and minor wounds (2). Internally, the leaves were used for gastrointestinal ailments and sore throats. Oral EPO is best known for its more recent use in the treatment of systemic diseases characterized by chronic inflammation, such as atopic eczema, and rheumatoid arthritis. The oil also is used for several women’s health conditions, including breast pain (mastalgia), menopausal and premenstrual symptoms.

The seeds of the evening primrose are rich in omega-6 essential fatty acids (EFAs), including linoleic acid and gamma-linolenic acid (GLA ). The therapeutic effects of EPO are attributed to the direct action of its component E FAs on immune cells, as well as their indirect effect on the synthesis of eicosanoids (e.g., prostaglandins, cytokines, cytokine mediators) (3,4) Dietary omega-3 and omega-6 E FAs can reduce the effects of eicosanoid actions, which have been implicated in various inflammatory and immunologic pathogeneses. (4)

Commercial preparations of EPO are available in capsule or liquid form. A single standardized 1-g capsule of a common formulation, containing 0.62 g linoleic acid, 0.08 g GLA , and 0.062 g oleic acid. Products may also be identified according to percent content of EFAs (e.g., 70% linoleic acid, 9% GLA ). In clinical trials, adult oral dosing for atopic dermatitis has ranged from 0.16 g to 0.64 g of GLA per day in divided doses, with treatment periods ranging from three to 16 weeks (5). Oral dosing in trials of children with atopic dermatitis has ranged from 0.08 g to 0.32 g GLA per day in divided doses (5). In trials of EPO for diabetic neuropathy, 0.36 g to 0.48 g GLA daily for six months has been used, and 0.5 g EPO containing 0.04 g GLA and 0.01 g vitamin E has been used for the treatment of cyclical mastalgia (6).

Uses of Evening Primrose Oil

Atopic eczema

Randomized controlled trials (RCT s) found no clear evidence of clinical benefit for topical or oral EPO for atopic dermatitis (5). A later meta-analysis found that the oil had a clinically modest but statistically significant beneficial effect on itch and pruritus in patients using it for four to eight weeks who were not also taking potent oral steroids (6) However, the meta-analysis included several unpublished, industry-sponsored trials that were excluded previously. Many of the studies had significant methodologic limitations, including small numbers; inadequate randomization; unclear blinding; and heterogeneity of dosing, duration, and patient characteristics.

Mastalgia, Menopause, and Premenstrual Symptoms

A systematic review of treatments for cyclical mastalgia found only three double-blind, placebo-controlled trials of EPO and one multicentre trial of GLA (an active ingredient of EPO) (7). The latter trial, which was of excellent quality, found that GLA was not superior to placebo, with or without additional antioxidant vitamins and minerals (8).

Pooling the four studies, the authors found no significant effect of EPO on mean pain scores compared with placebo (7). There is insufficient evidence to recommend the use of EPO in the treatment of mastalgia. Only one randomized, double-blind, placebo controlled multicentre trial has studied the effects of EPO in menopausal women (9). For a duration of six months, the participants took four capsules twice daily that contained either EPO (0.5 g EPO and 10 mg natural vitamin E per capsule) or placebo. The EPO showed no benefit in treating menopausal flushing compared with placebo.

A systematic review of four small, low-powered trials found that doses of EPO ranging from 3 to 6 g daily were not effective in improving overall symptoms of premenstrual syndrome (PMS) compared with placebo (10). Therefore, current evidence does not support a role for EPO in the management of menopause or PMS.

Diabetic Neuropathy

Although evidence to date is limited, several small studies suggest that GLA may be useful in patients with mild
to moderate diabetic neuropathy who achieve only partial relief from prescription drugs (11-13) However, larger methodologically sound studies are needed to confirm this assertion, and it is unclear whether such data may be extrapolated to EPO supplements.

Rheumatoid Arthritis

A Cochrane review comparing GLA (derived from evening primrose, borage, or black currant seed oil) with placebo in the treatment of rheumatoid arthritis found that current evidence is insufficient to make a reliable assessment of effectiveness (14).

Pregnancy

EPO is applied vaginally by many midwives to accelerate cervical ripening, shorten labour, and decrease the incidence of post-term pregnancies (15). However, no clinical RCT s support this use.

Safety

EPO is generally well tolerated, with reported minor adverse effects including gastrointestinal upset (e.g., abdominal pain, indigestion, nausea, softening of stools) and headaches (2,16,17). Two case reports involving only five patients in the 1980s raised speculation that EPO may exacerbate epilepsy or reduce the threshold for seizures in patients being treated with phenothiazines for schizophrenia (18,19). Although caution was advised for patients taking phenothiazine neuroleptics or anticonvulsants, neuroleptics themselves can induce seizures.

Keywords: atopic eczema; premenstrual mastalgia, premenstrual syndrome; menopause; rheumatoid arthritis; pregnancy

Monograph

http://www.ema.europa.eu/docs/en_GB/document_library/Herbal_-_Community_herbal_monograph/2012/04/WC500124923.pdf

Assessment report

http://www.ema.europa.eu/docs/en_GB/document_library/Herbal_-_HMPC_assessment_report/2012/04/WC500124922.pdf

References

http://www.ema.europa.eu/docs/en_GB/document_library/Herbal_-_List_of_references_supporting_the_assessment_report/2012/04/WC500124925.pdf

References

1. Blumenthal M, Brinckmann J, Wollschlaeger B. The ABC Clinical Guide to Herbs. Austin, Tex.: American Botanical Council; 2003.
2. Libster M. Delmar’s Integrative Herb Guide for Nurses. Albany, NY: Delmar/Thomson Learning; 2002:156-166.
3. Vassilopoulos D, Zurier RB, Rossetti RG, Tsokos GC. Clin Immunol Immunopathol. 1997;83(3):237-244.
4. Fan YY, Chapkin RS. J Nutr. 1998;128(9):1411-1414.
5. Hoare C, Li Wan Po A, Williams H. Health Technol Assess. 2000;4(37):1-191.
6. Morse NL, Clough PM. Curr. Pharm Biotechnol. 2006;7(6):503-524.
7. Srivastava A, Mansel RE, Arvind N, Prasad K, Dhar A, Chabra A. Breast. 2007;16(5):503-512.
8. Goyal A, Mansel RE; for the Efamast Study Group. Breast J. 2005;11(1):41-47.
9. Chenoy R, Hussain S, Tayob Y, O’Brien PM, Moss MY, Morse PF. BMJ. 1994;308(6927):501-503.
10. Stevinson C, Ernst E. Am J Obstet Gynecol. 2001;185(1):227-235.
11. Halat KM, Dennehy CE. J Am Board Fam Pract. 2003;16(1):47-57.
12. Keen H, Payan J, Allawi J, et al. Diabetes Care. 1993;16(1):8-15.
13. Jamal GA, Carmichael H. Diabet Med. 1990;7(4):319-323.
14. Little C, Parsons T. Herbal therapy for treating rheumatoid arthritis. Cochrane Database Syst Rev. 2001;(1):CD002948.
15. McFarlin BL, Gibson MH, O’Rear J, Harman P. J Nurse Midwifery.
1999;44(3):205-216.
16. Bamford JT, Gibson RW, Renier CM. J Am Acad Dermatol. 1985;13(6):959-965.
17. Barber A. Pharm J. 1988; 240:723-725.
18. Vaddadi KS. Prostaglandins Med. 1981;6(4):375-379.
19. Holman CP, Bell AF. J Orthomol Psychiatr. 1983;12:302-304.