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Herbal Monograph

Evening Primrose

Oenothera biennis L.

Onagraceae (Evening Primrose family)

Class 1 Anti-inflammatory Emmenagogue Nervine Demulcent

GLA-rich seed oil for inflammation, mastalgia, skin repair, and nerve health via the PGE1 pathway

Overview

Plant Description

Evening primrose is an erect, herbaceous biennial (occasionally short-lived perennial) growing 30-150 cm (1-5 feet) tall from a stout, fleshy taproot. In its first year, it forms a basal rosette of lanceolate to oblanceolate leaves, 10-30 cm long, with a prominent white midrib and slightly toothed or wavy margins. The second-year flowering stem is erect, stout, often reddish-tinged, and softly hairy. Stem leaves are alternate, sessile or short-petioled, lanceolate, 5-15 cm long. The flowers are the plant's most distinctive feature: large (2.5-5 cm diameter), four-petaled, bright lemon-yellow, sweetly fragrant, and open dramatically at dusk (hence 'evening' primrose), remaining open through the night for pollination by nocturnal moths (especially hawk moths, Sphingidae), then wilting by midday the following day. The flower has four sepals, four petals, eight stamens, and a four-branched cross-shaped stigma. Flowers are borne in a terminal, leafy spike from June through September. The fruit is an elongated, four-chambered capsule, 2-4 cm long, hairy, containing numerous tiny (1-2 mm), angular, dark reddish-brown to blackish seeds. Each plant may produce 10,000-70,000 seeds. The seeds are the primary medicinal part, yielding 14-17% fixed oil by weight when cold-pressed. The species name 'biennis' refers to the biennial life cycle.

Habitat

Evening primrose thrives in open, disturbed habitats with well-drained, sandy to gravelly soils. It is a quintessential pioneer species of roadsides, railway embankments, waste ground, vacant lots, riverbanks, sand dunes, gravel pits, and old fields. It tolerates poor, dry, nutrient-deficient soils and full sun exposure. The plant is drought-tolerant once established and does not compete well in closed, shaded vegetation. It colonizes disturbed ground rapidly from the persistent seed bank. It grows from sea level to approximately 2000 m elevation.

Distribution

Native to eastern and central North America, from Newfoundland and southern Canada south to Florida and Texas. Evening primrose was introduced to Europe in the early 17th century (first recorded in the Padua Botanical Garden, Italy, in 1612, likely brought from Virginia), initially as a curiosity and food plant ('German rampion' -- the first-year root was eaten as a vegetable). It subsequently naturalized extensively across Europe, temperate Asia, North Africa, South America, Australia, and New Zealand, becoming one of the most cosmopolitan of North American native plants. It is now cultivated commercially for seed oil production in many countries, with major production in China, Canada, the United Kingdom, and parts of continental Europe.

Parts Used

Seed oil (Evening Primrose Oil, EPO)

Preferred: Cold-pressed seed oil in soft gelatin capsules; liquid oil (refrigerated)

The cold-pressed fixed oil from ripe seeds is the primary modern medicinal preparation and the subject of virtually all clinical research. The oil is a rich source of gamma-linolenic acid (GLA, typically 8-14%) and linoleic acid (LA, 65-80%), both essential omega-6 fatty acids. GLA is the critical bioactive constituent. EPO was the first commercially significant plant source of GLA identified (by Rolf Aitchison and colleagues in the 1960s-1970s). The oil is pale yellow, with a mild nutty taste, and is typically supplied in soft gelatin capsules (usually 500 mg or 1000 mg, providing 40-50 mg or 80-100 mg GLA per capsule respectively). Oil quality depends on extraction method (cold-pressed preferred), seed quality, and storage conditions.

Seed (whole, ground)

Preferred: Ground seed powder; whole seeds as food supplement

Whole or ground seeds contain the oil along with fiber, protein, and minerals. Ground seeds may be used as a dietary supplement, though the oil in capsule form is far more commonly employed therapeutically. The seed contains approximately 14-17% oil by weight. Whole seeds pass through the digestive tract largely undigested unless ground or chewed thoroughly.

Root (first-year taproot)

Preferred: Fresh or dried root, decoction or poultice

The fleshy first-year root was used by Native American peoples and by European settlers as both food and medicine. Known as 'German rampion' when cultivated in Europe as a root vegetable. The root contains mucilage, tannins, and minerals. Traditional uses include poultice for wounds and bruises, and decoction for gastrointestinal complaints. The root is not used in modern clinical practice and has no significant presence in current herbal commerce.

Leaf and aerial parts

Preferred: Dried leaf infusion; fresh leaf poultice

The leaves and above-ground portions were used in various Native American and folk medicine traditions as teas, poultices, and washes. Leaves contain tannins (ellagitannins, especially oenothein B), flavonoids, phenolic acids, and mucilage. Oenothein B has demonstrated anti-inflammatory and antioxidant activity in preliminary research. The aerial parts have not been the subject of significant modern clinical research and are rarely used in contemporary herbal practice.

Key Constituents

Fatty acids (seed oil)

Gamma-linolenic acid (GLA, 18:3n-6) 8-14% of total seed oil fatty acids (typically 9-11% in commercial EPO); approximately 40-50 mg GLA per 500 mg capsule
Linoleic acid (LA, 18:2n-6) 65-80% of total seed oil fatty acids
Oleic acid (18:1n-9) 5-12% of total seed oil fatty acids
Palmitic acid (16:0) 6-10% of total seed oil fatty acids
Stearic acid (18:0) 1-3% of total seed oil fatty acids

The fatty acid composition of EPO, specifically the GLA content, is the basis for virtually all therapeutic applications. GLA provides a direct metabolic bypass of the delta-6-desaturase enzyme, which is the rate-limiting step in the conversion of dietary linoleic acid to the anti-inflammatory eicosanoid precursor DGLA. DGLA gives rise to PGE1 (a potent anti-inflammatory, vasodilatory, and antiplatelet prostaglandin) and 15-HETrE (which inhibits pro-inflammatory leukotriene B4 synthesis). This shift in eicosanoid balance -- from pro-inflammatory arachidonic acid-derived series-2 prostaglandins and series-4 leukotrienes toward anti-inflammatory PGE1 and 15-HETrE -- is the core pharmacological mechanism of EPO. Conditions characterized by impaired delta-6-desaturase activity (atopic eczema, diabetes, aging, premenstrual syndrome) are the primary therapeutic targets.

Phytosterols

Beta-sitosterol 50-70% of total sterol fraction; approximately 0.1-0.3% of crude seed oil
Campesterol 15-25% of total sterol fraction
Stigmasterol Minor sterol component, typically less than 5% of total sterols

Phytosterols in EPO contribute supplementary anti-inflammatory and membrane-stabilizing effects that complement the primary GLA-mediated eicosanoid pathway. While present at lower concentrations than the fatty acids, beta-sitosterol and campesterol may contribute meaningfully to the overall therapeutic effect, particularly in skin conditions and inflammatory states.

Polyphenols (primarily in leaves and aerial parts)

Oenothein B (macrocyclic ellagitannin) Up to 2-5% of dried leaf weight; major polyphenol of O. biennis leaves
Ellagic acid and gallic acid Present in leaves and seed coat; minor in refined oil
Flavonoids (quercetin, kaempferol glycosides) Minor components of leaves and flowers

The polyphenol constituents are primarily relevant to traditional preparations using the leaf and aerial parts (teas, poultices) rather than the modern seed oil. Oenothein B is of particular research interest for its anti-inflammatory, antimicrobial, and immunomodulating properties. These compounds are largely absent from refined EPO capsules, which highlights the difference between traditional whole-plant preparations and the modern isolated seed oil.

Tocopherols and tocotrienols (vitamin E)

Gamma-tocopherol Predominant tocopherol in EPO; approximately 15-35 mg per 100 g oil
Alpha-tocopherol Minor tocopherol; approximately 5-15 mg per 100 g oil

The natural tocopherol content serves a dual purpose: protecting the highly oxidation-prone polyunsaturated oil from rancidity (preservative function) and contributing modest antioxidant and anti-inflammatory effects. The gamma-tocopherol content may complement the anti-inflammatory activity of GLA. Adequate tocopherol content is an important quality marker for EPO products.

Mucilage and other carbohydrates (root and leaf)

Mucilaginous polysaccharides Present in root and leaf; not present in refined seed oil

Mucilage content is relevant only to traditional root and leaf preparations, where it contributes demulcent and soothing properties for topical and internal use. Not present in or relevant to EPO capsules.

Herbal Actions

Anti-inflammatory (primary)

Reduces inflammation

The primary pharmacological action of EPO, mediated through the GLA to DGLA to PGE1 pathway. GLA is elongated to DGLA (dihomo-gamma-linolenic acid) by elongase enzymes. DGLA serves as the precursor for prostaglandin E1 (PGE1), a potent anti-inflammatory prostaglandin that inhibits platelet aggregation, promotes vasodilation, and suppresses pro-inflammatory cytokine production. DGLA also yields 15-hydroxy-DGLA (15-HETrE), which inhibits the synthesis of pro-inflammatory leukotriene B4 from arachidonic acid. By shifting eicosanoid balance away from pro-inflammatory series-2 prostaglandins and series-4 leukotrienes toward anti-inflammatory PGE1 and 15-HETrE, EPO exerts a broad anti-inflammatory effect. This mechanism is supported by multiple clinical trials and is the basis for EPO use in eczema, mastalgia, rheumatoid arthritis, and diabetic neuropathy.

[1, 4, 5]
Emmenagogue (primary)

Stimulates or increases menstrual flow

EPO has a well-established traditional and clinical role in modulating menstrual and hormonal function. PGE1 derived from GLA influences uterine smooth muscle tone, hormonal receptor sensitivity, and the balance of prostaglandins involved in menstrual physiology. EPO is widely used for premenstrual syndrome (PMS), cyclical mastalgia (breast pain), and menstrual regularity. The mechanism involves normalization of the prostaglandin balance that governs uterine contractility, breast tissue fluid dynamics, and hormonal feedback. Clinical trials for cyclical mastalgia have shown the strongest evidence among EPO indications related to menstrual/hormonal function.

[1, 4, 7]
Nervine (secondary)

Supports and calms the nervous system

GLA-derived eicosanoids influence nerve membrane composition, nerve signal transduction, and neuronal blood flow. In diabetic neuropathy, impaired delta-6-desaturase activity leads to deficiency of GLA and DGLA in nerve membranes, contributing to demyelination and reduced nerve conduction velocity. GLA supplementation can restore nerve membrane fatty acid composition and improve nerve blood flow via PGE1-mediated vasodilation. Jamal et al. (1986) demonstrated significant improvement in nerve conduction parameters and neuropathy symptom scores with GLA supplementation in diabetic patients. This nervine action is specifically relevant to neuropathy rather than a general calming or sedative effect.

[4, 8, 9]
Demulcent (secondary)

Soothes and protects irritated mucous membranes

EPO functions as a systemic emollient and demulcent when taken internally. The essential fatty acids (GLA and LA) are incorporated into cell membranes and contribute to skin barrier function, mucous membrane integrity, and tissue hydration. GLA is a precursor to ceramides, which are critical components of the stratum corneum lipid barrier. In atopic eczema, impaired delta-6-desaturase activity leads to reduced GLA incorporation into skin lipids, contributing to transepidermal water loss and dry, irritated skin. Topical application of EPO also provides direct emollient effects. The whole-plant preparations (root, leaf) additionally contain mucilage that contributes conventional demulcent activity.

[1, 4, 5]
Antioxidant (secondary)

Prevents or slows oxidative damage to cells

EPO contains natural tocopherols (vitamin E, particularly gamma-tocopherol) that provide antioxidant protection. DGLA-derived 15-HETrE has indirect antioxidant effects by reducing inflammatory oxidative stress. The leaf and aerial parts contain significant polyphenol content (oenothein B, ellagic acid) with potent direct antioxidant activity, though these are absent from the refined seed oil. Beta-sitosterol in the oil also demonstrates antioxidant properties.

[1, 15]
Vulnerary (mild)

Promotes wound healing

EPO applied topically or taken internally supports wound healing through multiple mechanisms: GLA-derived PGE1 promotes microvascular blood flow to healing tissues, essential fatty acids support cell membrane regeneration, and phytosterols contribute anti-inflammatory effects at the wound site. Traditional Native American use of the root and leaf as wound poultices is consistent with this action. The seed oil has been investigated for post-surgical wound healing support.

[1, 16]
Hypotensive (mild)

Lowers blood pressure

PGE1 derived from GLA is a vasodilator and inhibitor of platelet aggregation. GLA supplementation has been associated with modest reductions in blood pressure in some clinical studies, particularly in hypertensive populations. The mechanism involves PGE1-mediated vascular smooth muscle relaxation and improved endothelial function. The effect is mild and unlikely to be clinically significant as a standalone antihypertensive intervention.

[1, 4]

Therapeutic Indications

Skin / Integumentary

supported

Atopic eczema (atopic dermatitis)

The most extensively studied indication for EPO, though results are mixed. The rationale is strong: atopic patients show impaired delta-6-desaturase activity, reduced GLA levels in plasma and breast milk, and elevated linoleic acid (indicating a metabolic block in LA-to-GLA conversion). Multiple early RCTs (Morse et al. 1989, Wright & Burton 1982) showed significant improvements in eczema severity, pruritus, and skin dryness. However, a 2013 Cochrane systematic review (Bamford et al.) including 27 RCTs found no convincing evidence of benefit over placebo for eczema. The German Commission E issued a negative monograph based on inconsistent eczema evidence. The discrepancy may reflect heterogeneity in patient populations (some subgroups with documented GLA deficiency may respond while unselected populations do not), product quality variation, dosing differences, and endpoint measurement. Current consensus: EPO may benefit a subpopulation of atopic eczema patients with demonstrable essential fatty acid deficiency, but it cannot be recommended as a universal eczema treatment.

[1, 3, 4, 5, 6]
traditional

Dry skin and general skin health

EPO supplementation is traditionally used and widely marketed for general skin health, skin hydration, and aging skin. GLA is incorporated into skin cell membranes and contributes to ceramide biosynthesis, a critical component of the stratum corneum barrier. Improvement in skin moisture, elasticity, and smoothness has been reported in open-label and small controlled studies. The evidence is largely traditional and empirical rather than rigorously established in large clinical trials.

[1, 4]
traditional

Wound healing support (topical and internal)

Traditional Native American use of evening primrose root and leaf as wound poultices is well documented. Modern application of EPO topically to wounds and surgical sites provides essential fatty acids for cell membrane regeneration and PGE1-mediated improvement in local blood flow. Limited formal clinical evidence specific to wound healing.

[1, 16]

Reproductive System

supported

Cyclical mastalgia (breast pain)

The strongest evidence-based indication for EPO. Cyclical mastalgia (breast pain associated with the menstrual cycle) has been the subject of multiple RCTs with generally positive results. Pruthi et al. (2010) conducted an RCT comparing EPO (standardized GLA content), vitamin E, and combined EPO+vitamin E for mastalgia, finding significant pain reduction in the EPO group. The Cardiff Breast Clinic in Wales routinely used EPO as first-line treatment for cyclical mastalgia for many years. The mechanism involves normalization of the fatty acid profile in breast tissue, modulation of prostaglandin synthesis affecting breast tissue fluid balance, and reduced sensitivity of breast tissue to hormonal fluctuations. GLA deficiency has been documented in women with mastalgia. Typical dosing: 3-4 g EPO daily (providing 240-320 mg GLA) for at least 3-4 menstrual cycles.

[1, 4, 7, 12]
supported

Premenstrual syndrome (PMS)

EPO is one of the most widely used herbal supplements for PMS symptoms (breast tenderness, bloating, irritability, mood changes). The rationale involves correction of GLA deficiency and normalization of prostaglandin balance affecting breast tissue sensitivity, fluid retention, and mood regulation. Several controlled studies have shown improvement in PMS symptoms, particularly breast tenderness and irritability. A systematic review by Budeiri et al. (1996) found modest evidence for benefit, though not all studies were positive. The strongest evidence is for breast-related PMS symptoms (consistent with mastalgia data). Used widely in clinical practice despite mixed formal evidence.

[1, 4, 13]
preliminary

Cervical ripening in late pregnancy

EPO is widely used by midwives and in natural childbirth preparation to support cervical ripening in late pregnancy (typically starting at 36-37 weeks gestation). The rationale involves PGE1- and PGE2-mediated effects on cervical collagen remodeling and softening. Dove & Johnson (1999) conducted an observational study finding no adverse effects but also no significant difference in labor outcomes. Ty-Torredes (2006) reported some evidence of improved cervical ripening scores. The practice is widespread in midwifery despite limited robust clinical trial evidence. EPO is taken orally and sometimes applied vaginally in late pregnancy.

[1, 14]

Nervous System

supported

Diabetic neuropathy

One of the better-supported clinical applications of GLA. In diabetes, delta-6-desaturase activity is impaired by hyperglycemia and insulin resistance, leading to GLA and DGLA deficiency in nerve membranes. This contributes to structural and functional nerve damage. Jamal et al. (1986) landmark RCT demonstrated significant improvement in nerve conduction velocity, thermal threshold, and neuropathy symptom scores with GLA supplementation (360 mg GLA/day as EPO) over 6 months compared to placebo. The larger multi-center trial by Keen et al. (1993) confirmed these findings in 111 patients. GLA supplementation restores nerve membrane fatty acid composition, improves endoneurial blood flow via PGE1, and may slow or partially reverse neuropathic changes. This indication has a clear biochemical rationale and consistent clinical evidence.

[4, 8, 9]

Musculoskeletal System

preliminary

Rheumatoid arthritis (adjunctive)

GLA supplementation has been investigated as an adjunctive anti-inflammatory treatment in rheumatoid arthritis. The rationale involves shifting eicosanoid synthesis from pro-inflammatory arachidonic acid metabolites to anti-inflammatory PGE1 and 15-HETrE. Leventhal et al. (1993) RCT using high-dose GLA (1.4 g/day from borage oil, equivalent to approximately 14 g EPO) found significant reduction in joint tenderness and swelling. Evidence using EPO specifically at standard doses (providing 240-360 mg GLA/day) is more limited, and higher GLA doses (achievable more easily with borage oil) may be needed for significant anti-inflammatory effects in RA. Considered adjunctive to standard rheumatological treatment.

[1, 4, 11]

Endocrine System

preliminary

Menopausal symptoms (hot flashes)

EPO is commonly used for menopausal hot flashes, though clinical evidence is mixed. Chenoy et al. (1994) conducted a double-blind, placebo-controlled RCT in 56 menopausal women and found no significant difference between EPO (4 g/day) and placebo for hot flash frequency or severity. However, the placebo response was high (significant improvement in both groups). Some practitioners report clinical benefit, particularly when combined with other interventions. The GLA-prostaglandin mechanism may influence thermoregulatory vasomotor function. Current evidence does not strongly support EPO as a standalone treatment for hot flashes, though it remains widely used.

[1, 10]
preliminary

Metabolic support in diabetes (adjunctive)

Beyond diabetic neuropathy specifically, GLA supplementation may benefit overall metabolic function in diabetes. Impaired delta-6-desaturase activity in diabetic patients leads to broad essential fatty acid metabolism disruption. GLA supplementation can partially correct this metabolic block, improving lipid profiles and vascular function. Evidence is primarily mechanistic and from small clinical studies.

[4, 8]

Cardiovascular System

preliminary

Mild hyperlipidemia and cardiovascular risk modification

GLA-derived PGE1 inhibits platelet aggregation and promotes vasodilation. EPO supplementation has been associated with modest improvements in lipid profiles (reduced total cholesterol, LDL, triglycerides) and blood pressure in some studies. Beta-sitosterol in EPO also competes with cholesterol for intestinal absorption. Effects are generally modest and EPO is not a primary cardiovascular intervention. May contribute to overall cardiovascular risk modification as part of a broader dietary fatty acid strategy.

[1, 4]

Immune System

preliminary

Atopic conditions and allergic diathesis

Atopic individuals often show impaired GLA metabolism. The shift in eicosanoid balance from pro-inflammatory to anti-inflammatory mediators may modulate the atopic immune response. PGE1 influences T-helper cell balance and suppresses IgE production. While the eczema evidence is inconsistent, the underlying immunological rationale for GLA in atopic conditions is sound. Some practitioners use EPO as a long-term constitutional remedy for atopic tendency.

[4, 5]

Energetics

Temperature

neutral

Moisture

slightly moist

Taste

blandsweet

Tissue States

hot/excitation, dry/atrophy

In Western herbal energetics, evening primrose oil is considered neutral in temperature and slightly moist in its tissue effect, reflecting its role as a systemic emollient and anti-inflammatory lipid. The oil has a bland to mildly sweet, nutty taste that does not strongly activate any of the traditional taste categories. The slightly moist quality reflects the oil's capacity to nourish dry, atrophic tissues -- particularly dry skin, depleted nerve sheaths, and desiccated mucous membranes. EPO is best indicated for conditions characterized by hot/excitation tissue states (inflammatory conditions such as eczema, mastalgia, inflammatory joint disease) and dry/atrophy tissue states (dry skin, nerve degeneration in diabetic neuropathy, depleted essential fatty acid status). The cooling, moistening, anti-inflammatory action of GLA-derived PGE1 is the energetic basis for EPO's therapeutic niche. Herbalists such as Matthew Wood and David Hoffmann place EPO in the category of nourishing, anti-inflammatory oils that restore tissue integrity in conditions of deficiency-driven inflammation. CAVEAT: Herbal energetics are interpretive frameworks within Western herbalism and are not standardized across all practitioners.

Traditional Uses

Native American (Ojibwe / Chippewa)

  • Root poultice applied externally for bruises, wounds, and skin eruptions
  • Root decoction taken internally for obesity and bowel complaints
  • Whole plant used as a healing poultice for boils and abscesses
  • Seeds and roots eaten as food

"Densmore (1928) documented Ojibwe use of Oenothera biennis root as a poultice soaked in warm water and applied to bruises and injuries to reduce swelling. The plant was considered a 'strength medicine' with broad healing properties."

[16, 17]

Native American (Cherokee)

  • Leaf tea (infusion of dried leaves) used as an internal remedy for various ailments
  • Root preparation for hemorrhoids
  • Hot root poultice for pain relief and swelling
  • Plant tea used to promote weight loss

"Hamel & Chiltoskey (1975) recorded Cherokee use of the leaf tea and root preparations for multiple conditions. The Cherokee name for the plant has been translated as referring to its use as a healing medicine."

[16]

Native American (Iroquois and other Eastern Woodland peoples)

  • Root preparations used for strength and as a general tonic
  • Poultice of the plant for hemorrhoids and piles
  • Root decoction for kidney and bladder complaints
  • First-year root eaten as a cooked vegetable

"Multiple Eastern Woodland peoples used Oenothera biennis medicinally and as food. The first-year root was widely harvested as a starchy root vegetable, eaten boiled or roasted."

[16]

Eclectic American medicine (19th-early 20th century)

  • Decoction or tincture of the whole plant for gastrointestinal spasm and colic
  • Used for hepatic torpor (sluggish liver) and dyspepsia
  • Topical application for skin diseases, eruptions, and wounds
  • Internal use for female reproductive complaints
  • Known as 'King's Cure-All' reflecting reputation as a broad-spectrum remedy

"John King, in the American Dispensatory (1854), described Oenothera biennis as possessing antispasmodic and astringent properties, useful for 'spasmodic asthma, gastric irritation, hepatic torpor, and chronic eruptions of the skin.' The common name 'King's Cure-All' likely refers to John King's promotion of the plant rather than any royal endorsement. Felter & Lloyd's King's American Dispensatory (1898) described the plant as 'a remedy of decided value in functional diseases of the liver and digestive apparatus.'"

[1, 18]

European folk medicine (17th-19th century)

  • First-year root cultivated and eaten as a vegetable ('German rampion' or 'Rapontika')
  • Root and leaf preparations for wounds and skin conditions
  • Infusion of leaves for cough and colds
  • Poultice of the plant for skin eruptions and sores

"Evening primrose was introduced to Europe from Virginia by 1612 and was initially cultivated in botanical gardens as a curiosity. It soon escaped and naturalized widely. The fleshy first-year root was cultivated as a root vegetable, particularly in Germany, where it was known as 'Rapontika' or 'Nachtkerze.' Culpeper and other European herbalists of the 17th-18th centuries used the plant for wounds and asthmatic complaints."

[1]

Modern Western phytotherapy (1980s-present)

  • Evening primrose oil (EPO) capsules for atopic eczema and dermatitis
  • EPO for premenstrual syndrome (breast tenderness, irritability, bloating)
  • EPO for cyclical mastalgia (breast pain)
  • EPO for diabetic neuropathy
  • EPO for general skin health and anti-aging
  • EPO for menopausal symptoms
  • EPO for rheumatoid arthritis (adjunctive)
  • EPO for cervical ripening in late pregnancy (midwifery practice)

"The modern therapeutic use of evening primrose oil began in the 1970s-1980s following the characterization of GLA as its key bioactive constituent by David Horrobin and colleagues. Horrobin's research on the role of essential fatty acid metabolism and prostaglandin synthesis in disease led to extensive investigation of EPO for conditions characterized by impaired delta-6-desaturase activity. The commercial product Efamol (standardized EPO) was launched in the early 1980s and became one of the best-selling herbal supplements worldwide."

[1, 4, 5]

Modern Research

narrative review

GLA metabolism and the delta-6-desaturase hypothesis

Comprehensive review by David Horrobin articulating the central hypothesis underlying EPO therapy: that impaired delta-6-desaturase (D6D) activity in various disease states leads to GLA deficiency, disrupted prostaglandin synthesis, and downstream inflammatory and metabolic consequences. Supplemental GLA from EPO bypasses this enzymatic block.

Findings: D6D activity is impaired by aging, diabetes, high saturated fat intake, alcohol, viral infections, atopic constitution, and zinc/magnesium/pyridoxine deficiency. This impairment reduces conversion of dietary linoleic acid to GLA, creating a 'metabolic bottleneck' that limits production of DGLA and anti-inflammatory PGE1. Supplemental GLA bypasses D6D entirely, restoring DGLA pools and PGE1 synthesis. This mechanism explains why conditions with documented D6D impairment (atopic eczema, diabetic neuropathy, PMS, mastalgia) are the most responsive to EPO therapy. The review also addressed the interconversion of DGLA to arachidonic acid (AA), noting that under normal circumstances, DGLA is preferentially converted to PGE1 rather than AA, so GLA supplementation does not increase pro-inflammatory AA-derived eicosanoids.

Limitations: Narrative review by the principal proponent of EPO therapy. Horrobin had commercial interests in Efamol (EPO product). Some claims regarding the breadth of D6D impairment in disease may be overstated. The review was published before several negative Cochrane reviews for eczema.

[4]

systematic review

Evening primrose oil for atopic eczema (Cochrane systematic review)

Cochrane systematic review evaluating oral EPO (and borage oil) for the treatment of eczema (atopic dermatitis). Included 27 studies of EPO involving over 1500 participants.

Findings: The review found no convincing evidence that oral EPO provides clinically meaningful improvement in eczema symptoms compared to placebo. Pooled analysis of global eczema severity scores, pruritus, and physician-assessed outcomes showed no statistically significant differences between EPO and placebo. However, significant heterogeneity existed among included studies in terms of population selection, EPO dose, product quality, treatment duration, and outcome measures. Some individual studies showed positive results while others did not. The authors noted that placebo oils (liquid paraffin, olive oil) used in control groups may themselves have had active effects on skin, potentially masking EPO benefit.

Limitations: Heterogeneity of included studies is a major limitation. Many studies were small and of variable quality. The use of active placebo oils (which may themselves affect skin) complicates interpretation. Patient selection criteria varied widely; studies did not consistently select for patients with demonstrated GLA deficiency. Dose ranges varied from 1-8 g/day EPO. The review treated eczema as a single entity rather than exploring subgroup responses.

[6]

rct

Evening primrose oil for cyclical mastalgia

Randomized controlled trial comparing EPO, vitamin E, and combined EPO + vitamin E for the treatment of cyclical mastalgia (cyclical breast pain) over 6 menstrual cycles.

Findings: Pruthi et al. (2010) enrolled 85 women with moderate-to-severe cyclical mastalgia. Participants receiving EPO (3 g/day providing approximately 270 mg GLA) showed significant reduction in breast pain severity compared to baseline, as measured by visual analog scale and daily breast pain diary. Response rates were comparable to vitamin E alone. The combination of EPO + vitamin E did not show additional benefit over either alone. The mechanism was attributed to correction of fatty acid imbalance in breast tissue and normalization of prostaglandin metabolism. Treatment was well tolerated with no significant adverse effects.

Limitations: Moderate sample size (n=85 across three treatment arms). No true placebo group (all arms received active treatment). Single-center study. Six menstrual cycles may be insufficient for full assessment. Measurement of breast pain is inherently subjective.

[7]

rct

GLA supplementation for diabetic neuropathy (landmark RCT)

Double-blind, placebo-controlled randomized trial evaluating gamma-linolenic acid (as evening primrose oil) for the treatment of diabetic peripheral neuropathy.

Findings: Jamal et al. (1986) demonstrated that GLA supplementation (360 mg/day as EPO, equivalent to approximately 4 g EPO daily) over 6 months produced statistically significant improvements in nerve conduction velocity, thermal discrimination threshold, tendon reflexes, and muscle strength in diabetic patients with established peripheral neuropathy, compared to placebo. Neuropathy symptom scores improved significantly in the treatment group. The findings provided strong support for the hypothesis that impaired essential fatty acid metabolism in diabetes contributes to neuropathic damage, and that GLA supplementation can partially reverse these changes.

Limitations: Relatively small sample size (n=22). Single-center study. Six-month duration; longer-term outcomes not assessed. Used composite neuropathy scores that may weight subjective and objective measures differently. Study was supported by Efamol Ltd.

[8]

rct

Multi-center trial of GLA for diabetic neuropathy

Large, multi-center, double-blind, placebo-controlled trial of GLA for diabetic neuropathy, designed to confirm and extend the findings of Jamal et al. (1986).

Findings: Keen et al. (1993) enrolled 111 patients with mild diabetic neuropathy across 7 centers. GLA (480 mg/day as EPO) administered for one year produced statistically significant improvements in 13 of 16 neurophysiological parameters measured, including nerve conduction velocities, thermal thresholds, and clinical neuropathy scores. Wrist and ankle median motor and sensory nerve conduction velocities improved significantly. Hot and cold thermal discrimination thresholds also improved. Muscle strength was better preserved in the GLA group. The improvements were more pronounced in patients with better glycemic control (HbA1c < 10%), suggesting that metabolic optimization enhances GLA efficacy.

Limitations: Sponsored by Scotia Pharmaceuticals (Efamol-related company). One-year duration; very long-term outcomes unknown. The 480 mg GLA dose was higher than typical consumer EPO supplementation. Benefit was greater in patients with better glycemic control, which may limit applicability in poorly controlled diabetes.

[9]

rct

Evening primrose oil for menopausal hot flashes (RCT)

Double-blind, randomized, placebo-controlled trial of EPO (500 mg capsules, 4 g/day) for the treatment of menopausal hot flashes in 56 symptomatic postmenopausal women over 6 months.

Findings: Chenoy et al. (1994) found no statistically significant difference between EPO and liquid paraffin placebo for the reduction of hot flash frequency or severity. Both groups showed substantial improvement from baseline (approximately 50% reduction in hot flash frequency), reflecting a strong placebo response. The maximum number of night sweats was slightly lower in the EPO group but the difference was not statistically significant. The authors concluded that EPO does not offer benefit beyond placebo for menopausal hot flashes.

Limitations: Small sample size (n=56). High placebo response rate making it difficult to detect modest active treatment effects. Liquid paraffin placebo may not be truly inert (fatty acid content). Single-center study. Six-month duration adequate but longer-term outcomes not assessed.

[10]

narrative review

Essential fatty acids in atopic eczema pathophysiology

Review examining the role of essential fatty acid metabolism abnormalities in the pathogenesis of atopic eczema and the rationale for GLA supplementation.

Findings: Morse et al. (2006) reviewed the evidence that atopic eczema patients have reduced blood levels of GLA, DGLA, and PGE1 metabolites, suggesting impaired delta-6-desaturase activity. Breast milk from atopic mothers also shows reduced GLA content, consistent with a systemic metabolic defect. The skin of eczema patients shows altered fatty acid composition with reduced ceramide content, contributing to impaired barrier function. EPO supplementation can correct the blood fatty acid profile and, in some studies, improve skin barrier parameters. The review noted that the variable clinical trial results may reflect the heterogeneity of atopic eczema as a condition, with only those patients who have demonstrable essential fatty acid deficiency likely to benefit from GLA supplementation.

Limitations: Narrative review. The author (Morse) was a long-time collaborator of Horrobin and advocate for EPO therapy. The review was published after the initial Cochrane review but does not fully address its negative findings. The subgroup hypothesis (only EFA-deficient patients benefit) has not been rigorously tested in prospective trials.

[5]

case series

Mastalgia treatment at the Cardiff Breast Clinic

Clinical experience and retrospective analysis of EPO use for cyclical mastalgia from the Cardiff Breast Clinic, which established EPO as a first-line treatment for this condition.

Findings: Gateley et al. (1992) reported on the Cardiff Breast Clinic's experience using EPO for cyclical mastalgia. In their series, approximately 45% of patients with cyclical mastalgia responded to EPO therapy (3 g/day for 3-6 months). Response rates were lower than danazol (70%) or bromocriptine (47%) but EPO had a far superior side-effect profile (less than 2% adverse effects compared to 30% for danazol). EPO was therefore recommended as first-line treatment due to its favorable risk-benefit ratio. The clinic's protocol established EPO dosing at 3 g/day (six 500 mg capsules, providing approximately 240 mg GLA) for a minimum of 4 menstrual cycles.

Limitations: Retrospective case series, not a randomized controlled trial. No true placebo comparison. The 45% response rate must be considered in light of the substantial placebo response rate (approximately 19%) seen in mastalgia studies. Assessment of response was clinician-determined.

[12]

rct

GLA for rheumatoid arthritis

Double-blind, randomized, placebo-controlled trial of high-dose GLA (1.4 g/day from borage oil) in patients with active rheumatoid arthritis.

Findings: Leventhal et al. (1993) randomized 37 patients with active RA to GLA 1.4 g/day (from borage oil) or placebo (cotton seed oil) for 24 weeks. The GLA group showed clinically significant reductions in joint tenderness (36% reduction vs 15% for placebo, P < 0.05), joint swelling, and morning stiffness. Global assessment by both patient and physician favored GLA. The anti-inflammatory effect was attributed to GLA-derived PGE1 and 15-HETrE suppression of pro-inflammatory eicosanoid synthesis. While this study used borage oil rather than EPO, the active constituent (GLA) is identical; EPO would require approximately 14 g/day to deliver equivalent GLA.

Limitations: Small sample size (n=37). Borage oil rather than EPO used (higher GLA concentration per gram). Achieving the equivalent GLA dose from EPO alone (approximately 14 g/day = 28 capsules) is impractical for most patients. Twenty-four-week duration; longer-term outcomes and radiographic progression not assessed.

[11]

cohort

Safety of evening primrose oil in pregnancy

Observational study evaluating the safety and effects of evening primrose oil supplementation in late pregnancy, addressing the widespread midwifery practice of using EPO for cervical ripening.

Findings: Dove & Johnson (1999) conducted a retrospective observational study of women who took EPO orally during late pregnancy compared to controls who did not. No significant adverse maternal or neonatal outcomes were associated with EPO use. No increase in postpartum hemorrhage, neonatal complications, or labor abnormalities was observed. However, the EPO group did not show statistically significant differences in cervical ripening, labor duration, or mode of delivery compared to controls. The study suggested that while EPO is safe in late pregnancy, evidence for efficacy in cervical ripening is lacking.

Limitations: Retrospective, observational design with inherent selection bias. Not randomized or blinded. Dosing was self-reported and variable. Sample size may have been insufficient to detect modest effects. The study could only assess safety in the context of third-trimester use.

[14]

in vitro

Oenothein B: anti-inflammatory and antimicrobial polyphenol from Oenothera leaves

Investigation of the pharmacological properties of oenothein B, the major polyphenol from O. biennis leaves, focusing on anti-inflammatory, antioxidant, and antimicrobial activities.

Findings: Kiss et al. (2011) demonstrated that oenothein B exhibits potent anti-inflammatory activity through inhibition of hyaluronidase, elastase, and collagenase enzymes; strong antioxidant capacity (DPPH radical scavenging IC50 comparable to ascorbic acid); and significant antimicrobial activity against Staphylococcus aureus (including MRSA strains). Oenothein B also inhibited NF-kB-mediated inflammatory signaling and showed immunomodulatory effects. These findings support the traditional use of O. biennis leaf preparations for wounds and skin conditions.

Limitations: In vitro study only; in vivo confirmation of these activities has not been established. Concentrations used in vitro may not be achievable through oral consumption of leaf tea. Oenothein B is present in leaf preparations but essentially absent from the refined seed oil that is the primary modern therapeutic form.

[15]

Preparations & Dosage

Capsule / Powder

Strength: Standard capsules: 500 mg or 1000 mg EPO per capsule. GLA content: 8-10% (40-50 mg or 80-100 mg per capsule). Some high-potency products are standardized to higher GLA (12-14%).

The standard and most widely used preparation. Evening primrose oil is encapsulated in soft gelatin capsules, typically containing 500 mg or 1000 mg of cold-pressed seed oil. Standard commercial EPO capsules provide approximately 8-10% GLA (40-50 mg per 500 mg capsule or 80-100 mg per 1000 mg capsule). Select products from reputable manufacturers that specify GLA content, cold-pressed extraction, and include natural tocopherols as antioxidant. Store capsules in a cool, dark place or refrigerator to prevent oxidation. Capsules may be swallowed whole or, for topical application, pierced and the oil applied directly to skin.

Adult:

3-6 g EPO per day (typically 6-12 capsules of 500 mg, or 3-6 capsules of 1000 mg) providing 240-480 mg GLA daily. For mastalgia: 3-4 g/day (240-320 mg GLA). For eczema: 4-8 g/day (320-640 mg GLA). For diabetic neuropathy: 4-6 g/day (360-480 mg GLA). For PMS: 2-4 g/day (160-320 mg GLA).

Frequency:

Divide daily dose into 2-3 doses taken with meals (fat-containing meals improve absorption of the oil)

Duration:

Minimum 8-12 weeks for clinical effect to become apparent. For mastalgia: at least 3-4 menstrual cycles. For diabetic neuropathy: 6-12 months minimum. May be used long-term.

Pediatric:

Children 1-12 years (for eczema): 2-4 g/day (scaled by body weight). Adolescents: adult dose. Use only under practitioner guidance.

Capsules are the standard preparation for therapeutic use and the form used in virtually all clinical trials. The encapsulated oil is protected from oxidation better than bottled liquid oil. Taking capsules with food (particularly fat-containing food) improves absorption of the oil-soluble constituents. The onset of clinical effect is slow (weeks to months) because GLA must be incorporated into cell membrane phospholipids and eicosanoid synthesis must equilibrate; patients should be counseled about this delay. Capsules can also be pierced and applied topically for localized skin conditions.

[1, 6, 7]

Standardized Extract

Strength: Standardized to 8-14% GLA. Common formulations: 500 mg capsule = 40-70 mg GLA; 1000 mg capsule = 80-140 mg GLA.

Commercially standardized EPO products guarantee a minimum GLA content, typically 8-10% GLA by weight. The most well-known standardized preparation is Efamol (standardized to 9% GLA). Some products are standardized to higher GLA content (up to 14%) through selective breeding of high-GLA cultivars. Look for products that specify: (1) GLA percentage, (2) cold-pressed extraction, (3) absence of solvent residues, (4) natural tocopherol content as antioxidant, (5) third-party testing for purity and potency.

Adult:

Dosing is based on GLA content: 240-480 mg GLA per day for most indications. Standardized products allow precise GLA dosing. Clinical trial doses have ranged from 240 mg GLA/day (mastalgia) to 480 mg GLA/day (diabetic neuropathy).

Frequency:

Two to three divided doses daily with meals

Duration:

Minimum 8-12 weeks; long-term use is safe and often necessary for chronic conditions

Pediatric:

Scale to body weight. Approximately 40-80 mg GLA per day for children under 12 for eczema.

Standardized products are preferred for clinical use because they guarantee consistent GLA delivery. The distinction between cold-pressed and solvent-extracted oils is clinically relevant: cold-pressing preserves natural tocopherols and avoids solvent residues, while solvent extraction may yield higher oil volumes but at potential cost to quality. Products should be stored in dark, cool conditions. Rancid oil (detectable by sharp, unpleasant odor when capsule is pierced) should not be consumed.

[1, 4, 19, 20]

Infusion (Tea)

Strength: 1:60 (approximately 4 g dried leaf per 240 mL water)

Traditional leaf tea preparation. Use 1-2 teaspoons (2-4 g) of dried evening primrose leaves per cup (240 mL) of boiling water. Steep for 10-15 minutes, covered. Strain and drink. The resulting tea has a mildly astringent, slightly bitter taste due to tannin content (including oenothein B).

Adult:

1 cup (240 mL) 2-3 times daily

Frequency:

Two to three times daily

Duration:

Short-term use for acute conditions; may be used for several weeks

Pediatric:

Half cup for children over 6 under practitioner guidance

Leaf infusion is a traditional preparation used by Native American and European folk traditions, distinct from the modern seed oil. The leaf tea provides polyphenols (oenothein B, ellagic acid), tannins, and flavonoids but does NOT contain significant amounts of GLA or the fatty acids that are the basis for modern EPO therapy. Leaf tea is appropriate for its astringent, anti-inflammatory polyphenol content (gastrointestinal soothing, mild wound wash) but should not be substituted for seed oil capsules when GLA is the therapeutic goal.

[16, 18]

Poultice

Strength: Fresh plant material applied directly; dried material reconstituted with warm water to poultice consistency

Traditional preparation using fresh or reconstituted dried root or leaves. For root poultice: clean and grate or mash fresh first-year root, apply directly to the affected area, and cover with clean cloth. For leaf poultice: bruise fresh leaves or reconstitute dried leaves with warm water, apply to the affected area, and secure with a bandage. Replace every 4-8 hours.

Adult:

Apply to affected area as needed, 2-3 times daily

Frequency:

Every 4-8 hours or as needed

Duration:

Until condition improves; typically several days

Pediatric:

Same as adult for external use

Poultice is the oldest preparation method for evening primrose, used extensively by Native American peoples (particularly Ojibwe) for wounds, bruises, boils, and skin eruptions. The root poultice provides mucilage (demulcent/soothing), tannins (astringent/wound-healing), and anti-inflammatory compounds. This preparation is based entirely on traditional use and has not been evaluated in modern clinical trials.

[16, 17]

Tincture

Strength: 1:5, 45-60% ethanol (dried herb); 1:2, 75% ethanol (fresh herb)

Tincture of fresh or dried aerial parts (leaf, stem, flower). Standard maceration: 1:5 ratio in 45-60% ethanol. Macerate fresh plant at 1:2 in 75% ethanol or dried plant at 1:5 in 45% ethanol for 2-4 weeks with daily agitation. Press and filter. Note: Tincture of the herb provides polyphenols and tannins but does NOT contain the seed oil or GLA in meaningful amounts. This is a traditional preparation distinct from modern EPO therapy.

Adult:

2-4 mL (40-80 drops) three times daily

Frequency:

Three times daily

Duration:

2-4 weeks for acute conditions; may be used longer for chronic complaints

Pediatric:

Not commonly used in children

Herbal tincture of evening primrose aerial parts is an Eclectic and traditional preparation that extracts the polyphenolic, tannin, and flavonoid constituents of the leaf and stem. This is NOT equivalent to EPO capsules and does not provide GLA. It has historical use for digestive complaints, liver support, and topical wound care (diluted). Rarely used in modern clinical practice, which has shifted almost entirely to the seed oil.

[1, 18]

Salve / Ointment

Strength: Approximately 75-80% EPO with 20-25% beeswax base

EPO can be incorporated into topical salve or ointment preparations. Warm 30 mL EPO with 7-10 g beeswax over gentle heat until beeswax melts. Remove from heat, stir continuously while cooling. Optionally add a few drops of vitamin E oil (additional antioxidant protection) and lavender essential oil. Pour into clean containers while still liquid. The resulting salve provides direct topical delivery of GLA and LA to the skin.

Adult:

Apply a thin layer to affected skin areas 2-3 times daily

Frequency:

Two to three times daily

Duration:

Ongoing as needed for skin conditions

Pediatric:

Same as adult for external use; suitable for children with eczema under practitioner guidance

Topical application of EPO provides direct delivery of GLA and LA to skin cells, supporting ceramide biosynthesis and skin barrier repair. Topical use is complementary to internal supplementation for skin conditions such as eczema. Some clinical studies have used topical EPO application in addition to oral supplementation. The salve should be stored in cool, dark conditions to prevent oil oxidation. Use within 3 months.

[1, 5]

Safety & Interactions

Class 1

Can be safely consumed when used appropriately (AHPA Botanical Safety Handbook)

Contraindications

absolute Known hypersensitivity to Oenothera biennis or other Onagraceae species

Individuals with confirmed allergy to evening primrose or related species should avoid EPO products. True allergy to EPO is extremely rare but has been reported.

relative Concurrent use with phenothiazine antipsychotics in patients with epilepsy (theoretical)

A theoretical concern has been raised that EPO may lower the seizure threshold, particularly when used concurrently with phenothiazine drugs (e.g., chlorpromazine, thioridazine) in patients with a history of temporal lobe epilepsy. This concern originated from a small number of case reports in the 1980s and early 1990s involving patients with schizophrenia on phenothiazines who were also taking EPO. However, subsequent analysis has found this concern to be poorly supported: a comprehensive review of available evidence concluded that EPO does not reliably lower seizure threshold, and the original case reports involved confounding variables (pre-existing seizure disorders, polypharmacy). Nevertheless, as a precautionary measure, EPO is conventionally avoided or used with caution in patients with active epilepsy who are taking phenothiazine medications.

Drug Interactions

Drug / Class Severity Mechanism
Warfarin, heparin, and other anticoagulants (Anticoagulants) theoretical GLA-derived PGE1 has mild antiplatelet activity. Theoretical additive anticoagulant effect when combined with pharmacological anticoagulants. However, this interaction has not been confirmed in clinical reports or controlled studies. A systematic review of herb-drug interactions found no documented cases of EPO-anticoagulant bleeding events.
Phenothiazine antipsychotics (chlorpromazine, thioridazine, etc.) (Antipsychotics (phenothiazines)) theoretical Historical concern that EPO may lower the seizure threshold, and that concurrent use with phenothiazines (which also lower seizure threshold) may additively increase seizure risk in susceptible individuals. The mechanism was hypothesized to involve prostaglandin effects on neuronal excitability. However, the evidence base is extremely limited and consists of a small number of poorly documented case reports with significant confounders.
Aspirin, clopidogrel, and other antiplatelet agents (Antiplatelet agents) theoretical Theoretical additive antiplatelet effect based on the antiplatelet properties of GLA-derived PGE1. No clinical case reports of bleeding events have been documented with this combination.
Anesthetic agents (pre-surgical) (Anesthetics) theoretical Theoretical concern regarding antiplatelet effects during surgery. The American Society of Anesthesiologists general recommendation to discontinue herbal supplements 2 weeks before elective surgery applies to EPO.

Pregnancy & Lactation

Pregnancy

likely safe

Lactation

likely safe

EPO has a long history of use in late pregnancy by midwives for cervical ripening, typically beginning at 36-37 weeks gestation. Dove & Johnson (1999) found no adverse maternal or neonatal outcomes in an observational study of EPO use during late pregnancy. The German Commission E monograph does not list pregnancy as a contraindication. The American Herbal Products Association Botanical Safety Handbook classifies EPO as Class 1 (safe when used appropriately) without a pregnancy restriction. GLA is a normal component of human breast milk and is considered safe during lactation; in fact, breast milk from atopic mothers is relatively deficient in GLA, suggesting that supplementation may be beneficial. While large-scale controlled safety studies in pregnancy are lacking, the overall safety profile is reassuring and EPO is widely regarded as safe during pregnancy and lactation by herbal practitioners and midwives. First-trimester use has been less studied than third-trimester use.

Adverse Effects

uncommon Mild gastrointestinal discomfort (nausea, soft stools, bloating, indigestion) — The most commonly reported side effect in clinical trials, typically mild and self-limiting. Occurs in approximately 2-5% of users. Usually resolves with dose reduction or when capsules are taken with food. Dividing the daily dose into multiple smaller doses throughout the day may reduce GI discomfort.
uncommon Headache — Mild headache has been reported in some clinical trial participants, though rates are generally comparable to placebo groups. Usually transient.
uncommon Soft stools or mild diarrhea — Related to the high oil content; more likely at higher doses (>4 g/day). Taking capsules with meals typically prevents this.
very-rare Allergic skin reaction (rash, urticaria) — Extremely rare. Discontinue use if allergic reaction occurs. True allergy to EPO is very uncommon.

References

Monograph Sources

  1. [1] Blumenthal M, Goldberg A, Brinckmann J (eds). Herbal Medicine: Expanded Commission E Monographs. American Botanical Council, Integrative Medicine Communications, Newton, MA (2000) . ISBN: 978-0967077215
  2. [2] Gardner Z, McGuffin M (eds). American Herbal Products Association Botanical Safety Handbook, 2nd edition. CRC Press, Boca Raton, FL (2013) . ISBN: 978-1466516946
  3. [3] German Federal Institute for Drugs and Medical Devices (BfArM). Commission E Monograph: Oenothera biennis (Evening Primrose Oil) — Negative Monograph. Bundesanzeiger (Federal Gazette), Germany (1994)
  4. [4] Horrobin DF. Essential fatty acid metabolism and its modification in atopic eczema. Am J Clin Nutr (2000) ; 71 (Suppl 1) : 367S-372S . DOI: 10.1093/ajcn/71.1.367S . PMID: 10617999
  5. [5] Morse NL, Clough PM. A meta-analysis of randomized, placebo-controlled clinical trials of Efamol evening primrose oil in atopic eczema. Where do we go from here in light of more recent discoveries?. Curr Pharm Biotechnol (2006) ; 7 : 503-524 . DOI: 10.2174/138920106779116946 . PMID: 17168667

Clinical Studies

  1. [6] Bamford JTM, Ray S, Musekiwa A, van Gool C, Humphreys R, Ernst E. Oral evening primrose oil and borage oil for eczema. Cochrane Database Syst Rev (2013) ; 4 : CD004416 . DOI: 10.1002/14651858.CD004416.pub2 . PMID: 23633319
  2. [7] Pruthi S, Wahner-Roedler DL, Torkelson CJ, Cha SS, Thicke LS, Hazelton JH, Bauer BA. Vitamin E and evening primrose oil for management of cyclical mastalgia: a randomized pilot study. Altern Med Rev (2010) ; 15 : 59-67 . PMID: 20359269
  3. [8] Jamal GA, Carmichael H. The effect of gamma-linolenic acid on human diabetic peripheral neuropathy: a double-blind placebo-controlled trial. Diabet Med (1986) ; 3 : 245-247 . DOI: 10.1111/j.1464-5491.1986.tb00750.x . PMID: 2951174
  4. [9] Keen H, Payan J, Allawi J, Walker J, Jamal GA, Weir AI, Henderson LM, Bissessar EA, Watkins PJ, Sampson M, Gale EAM, Scarpello J, Wing K, Boddie HG, Halliday D, Gulliford MC, Thomas PK. Treatment of diabetic neuropathy with gamma-linolenic acid. Diabetes Care (1993) ; 16 : 8-15 . DOI: 10.2337/diacare.16.1.8 . PMID: 8380713
  5. [10] Chenoy R, Hussain S, Tayob Y, O'Brien PMS, Moss MY, Morse PF. Effect of oral gamolenic acid from evening primrose oil on menopausal flushing. BMJ (1994) ; 308 : 501-503 . DOI: 10.1136/bmj.308.6927.501 . PMID: 8136666
  6. [11] Leventhal LJ, Boyce EG, Zurier RB. Treatment of rheumatoid arthritis with gammalinolenic acid. Ann Intern Med (1993) ; 119 : 867-873 . DOI: 10.7326/0003-4819-119-9-199311010-00001 . PMID: 8214997
  7. [12] Gateley CA, Miers M, Mansel RE, Hughes LE. Drug treatments for mastalgia: 17 years experience in the Cardiff Mastalgia Clinic. J R Soc Med (1992) ; 85 : 12-15 . PMID: 1548647
  8. [13] Budeiri D, Li Wan Po A, Dornan JC. Is evening primrose oil of value in the treatment of premenstrual syndrome?. Control Clin Trials (1996) ; 17 : 60-68 . DOI: 10.1016/0197-2456(95)00082-8 . PMID: 8721802
  9. [14] Dove D, Johnson P. Oral evening primrose oil: its effect on length of pregnancy and selected intrapartum outcomes in low-risk nulliparous women. J Nurse Midwifery (1999) ; 44 : 320-324 . DOI: 10.1016/S0091-2182(99)00055-3 . PMID: 10380443
  10. [15] Kiss AK, Bazylko A, Filipek A, Granica S, Jaszewska E, Kiarszys U, Kosmider A, Piwowarski J. Oenothein B's contribution to the anti-inflammatory and antioxidant activity of Epilobium sp.. Phytomedicine (2011) ; 18 : 557-560 . DOI: 10.1016/j.phymed.2010.10.016 . PMID: 21112747

Traditional Texts

  1. [16] Moerman DE. Native American Ethnobotany. Timber Press, Portland, OR (1998) . ISBN: 978-0881924534
  2. [17] Densmore F. Uses of Plants by the Chippewa Indians. Forty-Fourth Annual Report of the Bureau of American Ethnology, Smithsonian Institution, Washington, DC (1928) : 275-397
  3. [18] Felter HW, Lloyd JU. King's American Dispensatory, 18th edition. Ohio Valley Company, Cincinnati, OH (1898)

Pharmacopeias & Reviews

  1. [19] European Medicines Agency (EMA), Committee on Herbal Medicinal Products (HMPC). European Union herbal monograph on Oenothera biennis L. or Oenothera lamarckiana L., oleum. EMA/HMPC/572828/2013 (2018)
  2. [20] British Pharmacopoeia Commission. British Pharmacopoeia: Evening Primrose Oil. The Stationery Office, London (2024)

Last updated: 2026-03-02 | Status: review

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Full botanical illustration of Oenothera biennis L.

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