IngredientsGamma-linolenic acid (GLA, cis-6, cis-9, cis-12-octadecatrienoic acid) is a conditionally essential fatty acid of the n-6 family. It is a polyunsaturated fatty acid (PUFA) with three cis (Z) double bonds — the first from the methyl end being at the omega-6 (ω-6) position — classified in shorthand as 18:3n-6. Its molecular weight is 278.4296 g/mol, molecular formula C₁₈H₃₀O₂, and its IUPAC name is (6Z,9Z,12Z)-octadeca-6,9,12-trienoic acid (CAS registry number 506-26-3; PubChem 5280933).
Gamma-linolenic acid was first isolated by Heiduschka A. and Luft K. in 1919 from the seed oil of Oenothera biennis (evening primrose). Its structure was first proposed by Eibner A. and Luft K. in 1927 and later confirmed by Riley J.P. in 1949. GLA was synthesized in 1961 by Osbond J.M. et al. The compound is also known by several synonyms: gamolenic acid (its International Nonproprietary Name), cis-6,cis-9,cis-12-octadecatrienoic acid, and 18:3n-6. Gamma-linolenic acid is an isomer of alpha-linolenic acid, but whereas alpha-linolenic acid belongs to the omega-3 series, GLA is strictly an omega-6 fatty acid.
GLA is widely distributed in the plant kingdom in trace amounts and is not present in major commercial vegetable seed oils. It is present in seeds of many species belonging to families Aceraceae, Boraginaceae, Cannabinaceae, Liliaceae, Onagraceae, Ranunculaceae, Saxifragaceae, and Scrophulariaceae. A very limited number of plant sources have been commercialized in the last 30 years as a source of GLA, mainly in the health food industry and to a limited extent in pharmaceutical, pet food, and cosmetic industries. These include oils of borage, black currant, evening primrose, and recently hemp.
GLA is found in certain plant seed oils, notably evening primrose oil and borage oil, where it constitutes about 8–10% and 20–23% of total fatty acids, respectively. Borage oil is the richest supplemental source (17 to 25 percent GLA), followed by black currant oil (15 to 20 percent) and evening primrose oil (7 to 10 percent). Beyond seed oils, spirulina lipid contains 18–21% GLA; however, only 7.8% of spirulina is lipid by dry mass, so the overall GLA content by dry mass is closer to 1.23%. According to the USDA Standard Release, GLA is present in hemp seeds (1.34% by mass), some vegetable oil products (0.59% in soft margarine), and some meats (0.1% in chicken skin). GLA is found in moderate amounts in human breast milk, making it a significant natural source during infancy.
Some fungi and algae form GLA-rich lipid stores, examples being strains of Rhizopus, Mortierella, Mucor, and Spirulina.
Evening primrose oil supplements come as softgels, capsules, and liquids, and are also added to creams and ointments for topical application. The seed oil of the evening primrose (EPO) has been widely used commercially as a component of foods, as a nutritional supplement, as an ingredient of cosmetic, skin care and hair care products, and as a pharmaceutical. GLA can also be obtained in more concentrated forms via purified preparations from borage or black currant seed oil, which allow higher per-capsule doses than those achievable from evening primrose oil alone.
Many Native American groups used evening primrose medicinally, including the Anishinaabe, Cherokee, Iroquois, Ojibwas, and Potawatomi. Many groups used tea from the plant to improve energy levels and aid in weight loss. They also made a poultice from the plant to treat bruises, piles, and boils. They chewed the roots and rubbed them onto the muscles to improve strength. The plant was also sometimes used internally to treat bowel and menstrual pain.
Native Americans used the leaves and bark of evening primrose as a sedative and astringent; it was given for stomach and liver complaints as well as disorders of the female reproductive system. The Flambeau Ojibwe tribe soaked the whole plant in warm water to make a poultice for healing bruises and to overcome skin problems. Evening primrose was used by Native Americans to heal wounds, bruises, and to soothe swollen skin; they would eat the leaves to help with sore throats and stomach issues.
In the 17th century, evening primrose was introduced to European botanical gardens as an ornamental, and its oil became a popular folk remedy, earning the plant one of its common names, "King's Cure-All." The Cherokee, Iroquois, Ojibwas, and Potawatomi were among several Native American tribes that used evening primrose for both food and medicinal purposes; they ate the cooked greens when young, made a tea for overfatness, and a hot root poultice for piles. The bark and leaves are astringent and sedative and were used for the treatment of gastrointestinal disorders, whooping cough, and asthma.
It is important to note that traditional uses concerned the whole plant — leaves, roots, bark, and stems — not the isolated fatty acid. GLA was first isolated in 1919 from the oil of the evening primrose plant, a wildflower with a long history of use in folk remedies including as a treatment for pain, swelling, skin disorders, and menstrual pain. The connection between these traditional uses and GLA specifically was only recognized in the 20th century, once the chemistry and biochemistry of the fatty acid had been established.
The human body produces GLA from linoleic acid (LA). This reaction is catalyzed by Δ6-desaturase (D6D), an enzyme that allows the creation of a double bond on the sixth carbon counting from the carboxyl terminus. Dietary GLA bypasses the rate-limiting Δ6 desaturation step and is quickly elongated to DGLA by elongase, with only a very limited amount being desaturated to arachidonic acid (AA) by Δ5 desaturase.
A lack of GLA can occur when there is a reduction in the efficiency of the D6D conversion (for instance, as people grow older or when there are specific dietary deficiencies) or in disease states wherein there is excessive consumption of GLA metabolites. Factors known to reduce D6D activity include aging, diabetes, nutritional deficiencies (particularly of zinc, magnesium, and vitamins B6 and C), high intake of trans-fatty acids, and excessive alcohol consumption.
GLA may be elongated to dihomo-gamma-linolenic acid (DGLA) by an elongase enzyme. Δ5-desaturase can then metabolize dihomo-gamma-linolenic acid to arachidonic acid. DGLA is the precursor of the prostaglandin PGH1, which in turn forms PGE1 and the thromboxane TXA1. Both PGE1 and TXA1 are anti-inflammatory; TXA1 induces vasodilation and inhibits platelet aggregation, modulating (reducing) the pro-inflammatory properties of thromboxane TXA2. PGE1 has a role in regulation of immune system function. Unlike arachidonic acid and EPA, DGLA cannot yield leukotrienes; however, it can inhibit the formation of pro-inflammatory leukotrienes from arachidonic acid.
Upon stimulation, DGLA can be converted by inflammatory cells to 15-(S)-hydroxy-8,11,13-eicosatrienoic acid (15-HETrE) and prostaglandin E1. This is noteworthy because these compounds possess both anti-inflammatory and antiproliferative properties. DGLA can be converted to PGE1 via the cyclooxygenase pathway and/or converted to 15-HETrE via the 15-lipoxygenase pathway. 15-HETrE is capable of inhibiting the formation of AA-derived 5-lipoxygenase (pro-inflammatory) metabolites.
Anti-inflammatory mediators such as prostaglandin E1 (PGE1) and 15-HETrE, originating from GLA metabolism, are crucial in regulating fever, smooth muscle contraction, and immune modulation. GLA also influences COX and LOX activity by promoting the synthesis of anti-inflammatory molecules, thereby contributing to immune regulation.
When acting on GLA, arachidonate 5-lipoxygenase produces no leukotrienes, and the conversion by the enzyme of arachidonic acid to leukotrienes is inhibited. This dual action — generating anti-inflammatory series-1 prostaglandins through one arm, while simultaneously suppressing pro-inflammatory leukotriene synthesis through another — provides GLA with a distinctive anti-inflammatory mechanism that distinguishes it from most other omega-6 fatty acids.
Recent studies demonstrate that dietary GLA increases the content of its elongase product, DGLA, within cell membranes without concomitant changes in arachidonic acid (AA). GLA and DGLA increased in serum lipids of subjects supplemented with 3.0 and 6.0 g/d; GLA supplementation with 3.0 and 6.0 g/d also resulted in an enrichment of DGLA in neutrophil phospholipids but no change in GLA or AA levels. This preferential enrichment of DGLA — rather than its conversion to pro-inflammatory AA — is considered a key mechanism underlying GLA's clinical effects.
The most thoroughly studied clinical application of GLA is in rheumatoid arthritis (RA). To assess the clinical efficacy and adverse effects of GLA, a plant seed oil-derived unsaturated fatty acid that suppresses inflammation and joint tissue injury in animal models, fifty-six patients with active RA were randomized to treatment groups in a 6-month, double-blind trial of GLA versus placebo. This was followed by a 6-month, single-blind trial during which all patients received GLA. Patients were treated with 2.8 g/day of GLA as the free fatty acid or with sunflower seed oil (placebo) administered in identical capsules.
Treatment with GLA for 6 months resulted in statistically significant and clinically relevant reductions in the signs and symptoms of disease activity in patients with RA. Overall meaningful responses (at least 25% improvement in 4 measures) were also better in the GLA treatment group (14 of 22 patients versus 4 of 19 in the placebo group; P = 0.015). Patients taking GLA during the entire study showed progressive improvement during the second 6 months; 16 of 21 patients showed meaningful improvement at 12 months compared with study entry.
GLA at doses used in this study was described as a well-tolerated and effective treatment for active RA. GLA is available as a component of several plant seed oils and is usually taken in far lower doses than were used in this trial. It is not approved in the United States for the treatment of any condition. An earlier trial by Leventhal et al. (1993, Annals of Internal Medicine) at the University of Pennsylvania also examined borage seed oil at approximately 1,100 mg GLA/day and reported reductions in synovitis. However, the overall evidence base for GLA in RA consists of a limited number of relatively small trials, and longer-term, larger confirmatory studies have not been completed.
Atopic dermatitis (AD) has been related to a deficiency of delta-6-desaturase, an enzyme responsible for the conversion of linoleic acid to gamma-linolenic acid (GLA). As a result of reduced enzyme activity of delta-6-desaturase, high levels of LA and low levels of GLA have been observed in AD patients. This provided a compelling mechanistic rationale for supplementation trials.
One open study included 21 patients with AD, to whom EPO (4–6 g) was administered daily for 12 weeks. A significant increase in plasma GLA and DGLA levels and a decrease in the objective SCORAD were observed 4 and 12 weeks after initiation of EPO treatment. GLA is reportedly efficacious for treating transepidermal water loss (TEWL) and epidermal hyper-proliferation. In one study, GLA-containing food was given to adults with dry skin or mild atopic dermatitis; beneficial effects on the TEWL index were recognized, and the efficacy of GLA was statistically significant especially in subjects with pro-inflammatory features.
A number of studies tested GLA-rich oils for treating atopic dermatitis. Initially, trials from the 1980s and 1990s indicated that GLA-rich oils could be useful for relieving symptoms. Multiple studies showed that GLA supplementation (at durations of at least four weeks) could reduce dermatitis symptoms in both children and adults, providing relief from itchiness and redness. These benefits appeared to be due to the generation of anti-inflammatory GLA metabolites improving skin barrier function.
However, the overall evidence picture for eczema is mixed. GLA has been widely marketed for addressing eczema, but current research suggests that it may not provide significant benefits for this condition. A meta-analysis of 27 studies on improvement of atopic dermatitis symptoms yielded mixed/negative results. The licensed evening primrose oil products marketed specifically for atopic eczema in the United Kingdom (Epogam and Efamast) were withdrawn from clinical use in 2002 after re-evaluation of the benefit/risk ratio. The current scientific consensus characterizes the evidence as mixed.
GLA has been studied for its possible benefits for diabetic neuropathy. Diabetic patients have abnormalities of essential fatty acid metabolism and therefore may require higher amounts of essential fatty acids. GLA and linoleic acid are both essential components of myelin and the neuronal cell membrane, and GLA has provided positive results in the treatment of experimental diabetes.
Two of three randomized controlled trials showed positive effects of GLA in diabetic neuropathy. Two of the trials demonstrated, with GLA at 360 mg/day for 6 months and 480 mg/day for 1 year, statistically significant improvements in neuropathy scores, nerve conduction velocities, and action potentials. A review of three randomized, controlled trials suggested evening primrose oil might improve symptoms of diabetic neuropathy. Dosages in these trials ranged from 360 to 480 mg GLA daily. Few adverse effects were noted in these trials, and there was no increase in blood glucose levels.
More recently, gamma-linolenic acid derived from evening primrose oil was found noninferior to alpha-lipoic acid for reducing pain in patients with diabetic neuropathy. Nevertheless, the supplement is primarily associated with potential benefits for diabetic neuropathy, although conclusive evidence for its effectiveness remains limited. The evidence is promising but comes from a small number of trials with limited sample sizes.
Among 10 clinical studies on mastalgia (breast pain), seven showed the priority of evening primrose oil over other treatments. Wide-ranging doses of 0.27 g to 6.48 g GLA per day have been used in clinical studies in mastalgia. However, more recent evidence has tempered earlier enthusiasm. Current research suggests that GLA may not provide significant benefits for cyclic mastalgia.
One randomized, multicenter, controlled double-blind trial tested GLA in combination with other nutrients in women with cyclic breast pain associated with fibrocystic breast changes. Women were randomized to receive a liquid formulation (1 g GLA, 750 μg iodine, and 70 μg selenium) or control formula daily for three cycles. Breast pain scores decreased similarly in both groups (−32.2% experimental vs. −33.1% control, p = 0.64). Nodularity was reduced in the experimental but not the control group. Among women who continued pain medication, the amount was reduced in the experimental group relative to controls. This study did not isolate the effect of GLA alone.
For premenstrual syndrome (PMS) more broadly, study results vary: some show benefit, others do not. The evidence for GLA's effect on menopausal vasomotor symptoms (hot flashes) is similarly mixed and limited.
Gamma-linolenic acid has been investigated for potential cardiovascular benefits. Studies indicate that GLA supplementation may help lower blood pressure, improve lipid profiles, and reduce the risk of cardiovascular diseases. These effects are likely mediated through the anti-inflammatory and vasodilatory properties of PGE1, as well as the potential inhibition of platelet aggregation. Preliminary data suggest benefit in some lipid profiles, but robust, large-scale outcome trials in cardiovascular disease are lacking. The mechanistic plausibility via DGLA-derived eicosanoids is well-established; the clinical evidence, however, is sparse.
Gamma-linolenic acid demonstrates promising potential in cancer therapy by selectively inducing apoptosis in cancer cells while sparing normal cells. It has been shown to disrupt the cancer cell cycle and promote cell death. GLA may help prevent inflammatory diseases by converting into dihomo-DGLA, which produces powerful anti-inflammatory agents. Given its anti-inflammatory and immune-modulating effects, GLA holds promise as an adjunct in cancer therapy, although its selective anticancer properties require further investigation. The current evidence in oncology is predominantly preclinical (in vitro and animal models); robust human clinical trial data in oncology are lacking.
Preliminary data suggest benefit for ocular surface diseases such as dry eye. GLA's proposed mechanism in this context is the modulation of inflammatory eicosanoids in the lacrimal gland and ocular surface. The evidence base remains small, consisting of preliminary studies only.
In multiple sclerosis patients, evening primrose oil may improve fatigue and quality of life, and along with hemp seed and a diet high in antioxidants, it may improve clinical and immunological parameters. This evidence is early-stage and has not been replicated in large, well-powered trials.
GLA is commercially available primarily in the form of softgel capsules of plant seed oils, most commonly evening primrose oil, borage seed oil, and black currant seed oil. Evening primrose oil has been administered orally in clinical trials at doses between 1 and 8 g/day in adults and 2 and 4 g/day in children. The typical content of GLA in the oil is 8% to 10%.
Dosages in published clinical studies vary substantially by indication:
For diabetic neuropathy, the typical dose is about 400 to 600 mg GLA daily (approximately 4 to 6 g of evening primrose or 2 to 3 g of borage oil).
It is important to distinguish between the dose of the whole oil preparation and the actual delivered GLA dose. Borage oil, as the richest supplemental source, contains 17 to 25 percent GLA, followed by black currant oil at 15 to 20 percent, and evening primrose oil at 7 to 10 percent. Consumers and clinicians should verify the amount of actual GLA per capsule rather than the amount of total oil.
While GLA is generally well-tolerated by most people, common side effects can include mild digestive issues, headaches, and nausea, especially at higher doses. GLA is generally well tolerated and any reported side effects — such as headache, nausea, diarrhoea, acid reflux and bloating — are usually mild. In one clinical study, the physician confirmed that none of the subjects showed any noteworthy side effects.
Gamma-linolenic acid might slow blood clotting. Taking GLA along with medications that also slow clotting might increase the chances of bruising and bleeding. Some medications that slow blood clotting include aspirin, clopidogrel (Plavix), diclofenac, ibuprofen, naproxen, dalteparin (Fragmin), enoxaparin (Lovenox), heparin, warfarin (Coumadin), and others. Patients taking antiplatelet agents or anticoagulants should use EPO cautiously or not at all.
Taking gamma-linolenic acid with phenothiazines might increase the risk of having a seizure in some people. Some phenothiazines include chlorpromazine (Thorazine), fluphenazine (Prolixin), trifluoperazine (Stelazine), thioridazine (Mellaril), and others. If you have epilepsy or schizophrenia, evening primrose oil may lower your seizure threshold. The same risk applies if you take phenothiazine medications for serious mental health conditions.
Uncertified borage oil supplements may contain liver-toxic pyrrolizidine alkaloids (PAs). Some sources of GLA, specifically borage seed oil, can contain compounds called pyrrolizidine alkaloids (PAs). These compounds can be toxic to the liver, especially when consumed in high doses or for prolonged periods. Borage seed oil has the highest GLA potency per capsule but must be labeled PA-free with validated testing to avoid pyrrolizidine alkaloids. Brands that disclose PA testing methods or carry third-party certifications should be favored.
Theoretically, the use of nonsteroidal anti-inflammatory drugs (NSAIDs) may counteract the effect of EPO, since NSAIDs inhibit cyclooxygenase enzymes required for the conversion of DGLA to the anti-inflammatory series-1 prostaglandins that mediate GLA's principal effects.
EPO (and by extension, its GLA content) may increase the effectiveness of ceftazidime, chemotherapy agents, and cyclosporine and may interact with phenothiazines, thus causing an increase in seizures.
Information regarding safety and efficacy in pregnancy and lactation is lacking. A case report exists of transient petechiae in a newborn following oral and intravaginal use of evening primrose oil for cervical ripening for a week prior to the infant's birth. GLA should not be taken if a person has a seizure disorder such as epilepsy, a bleeding disorder, or if surgery is planned. It should not be taken during pregnancy. The safety of GLA in babies and younger children has not been established.
As a highly polyunsaturated fatty acid, GLA is prone to oxidative rancidity. High-quality oil (preferably certified organic), packaged in light-resistant containers, refrigerated, and marked with a freshness date should be obtained to avoid rancidity. Rancid or oxidized oils may have altered and potentially harmful biological activity.
Clinical trials show mixed results, with some studies showing benefits for specific conditions while others find no significant effects. Early positive findings have led to the supplement being considered overhyped in some analyses. While GLA is a precursor to anti-inflammatory compounds, its conversion rate in the body can be variable and limited. The anti-inflammatory pathway from GLA to DGLA to PGE1 provides a plausible biological explanation for clinical effects, but "plausible mechanism plus mixed results" is a common pattern in supplement research, and the jury is still out.
The strongest clinical evidence exists for rheumatoid arthritis (several small-to-moderate RCTs with positive findings at high doses) and diabetic neuropathy (two of three RCTs showing benefit at 360–480 mg GLA/day). Evidence for atopic dermatitis is mixed, with early positive trials followed by negative meta-analyses. Evidence for mastalgia, PMS, cardiovascular effects, and most other applications is preliminary, inconsistent, or based on very small studies. Evidence in oncology and neurology remains predominantly preclinical. Overall, evidence suggests that evening primrose oil may be effective for treating rheumatoid arthritis, injection site skin reactions, and diabetic neuropathy, but is lacking to support its use in atopic eczema/dermatitis syndrome, menopausal vasomotor symptoms, mastalgia, or multiple sclerosis.
Health conditions that GLA (gamma linolenic acid) may help support.
Clinical data suggest GLA supplementation may reduce acne lesions, partly by restoring the skin barrier and reducing inflammatory mediators. A 10-week trial found that 2,000 mg/day of borage oil (containing ~400 mg GLA) significantly decreased breakouts and acne-related lesions. GLA is metabolized to DGLA, a precursor of anti-inflammatory prostaglandin E1 that suppresses pro-inflammatory cytokines. Evidence remains preliminary and more rigorous trials are needed.
GLA reduces platelet aggregation and thromboxane B2 while increasing vascular prostacyclin—a profile that supports arterial health and reduces atherosclerotic risk factors. Clinical trials and observational data link GLA/DGLA levels to reduced cardiovascular events. Limited evidence suggests GLA may help prevent clogged arteries.
GLA is among the best-studied natural supplements for rheumatoid arthritis, with multiple randomized controlled trials demonstrating clinically relevant reductions in joint pain, swelling, and disease activity. A key 1996 double-blind RCT (n=56) found 2.8 g/day GLA over 6 months produced significantly greater improvement than placebo. Evidence is particularly strong compared to most herbal/supplement interventions for RA.
GLA has been investigated in clinical trials for ADHD, with the 1989 Arnold et al. placebo-controlled comparison to D-amphetamine being the earliest RCT. More recent omega-3/GLA combination trials show weak to modest evidence of benefit. GLA alone has generally not demonstrated robust efficacy in ADHD, but its role as an adjuvant anti-inflammatory agent in combination with omega-3s continues to be investigated.
GLA, an omega-6 PUFA found in borage, evening primrose, and black currant oils, is metabolized to dihomo-gamma-linolenic acid (DGLA), which produces anti-inflammatory eicosanoids. Clinical trials in rheumatoid arthritis have shown reductions in joint tenderness and swelling. It has been studied as adjunctive therapy in multiple autoimmune-mediated inflammatory conditions.
GLA supplementation significantly reduces platelet aggregation and serum thromboxane B2—a platelet activator—while increasing bleeding time and vascular prostacyclin, a profile consistent with reduced thrombotic risk. A 4-month clinical study in hyperlipidemic patients documented ~45% reduction in platelet aggregation with GLA.
GLA combined with EPA has lowered blood pressure in two clinical trials involving over 100 subjects. A 3-month GLA supplementation study in older subjects was associated with beneficial reduction in arterial hypertension. GLA is also theorized to reduce blood pressure via PGE1-mediated vasodilation, with supportive animal data showing dose-dependent BP reduction.
GLA's primary connection to blood sugar is through diabetic neuropathy: diabetics have an impaired ability to convert linoleic acid to GLA, and GLA supplementation corrects the downstream deficit in nerve membrane lipids. GLA itself does not directly lower blood glucose but addresses glucose-related nerve damage and metabolic dysregulation downstream of glycemic disruption.
A pilot RCT found that GLA combined with EPA and calcium significantly preserved and increased lumbar spine and femoral bone mineral density (BMD) in elderly women versus calcium alone over 18–36 months. Animal work shows GLA and EPA enhance calcium absorption and deposition in bone. Evidence is limited but encouraging.
Clinical evidence shows GLA supplementation reduces total cholesterol and LDL-cholesterol while raising HDL-cholesterol in hyperlipidemic patients. Studies show significant cholesterol improvements alongside triglyceride reductions. Effects appear dose-dependent and more pronounced with longer supplementation periods.
GLA exerts documented anti-inflammatory effects through conversion to DGLA and subsequent production of prostaglandin E1 (PGE1) and 15-OH-DGLA, which inhibit pro-inflammatory eicosanoids. Multiple clinical trials in inflammatory conditions (RA, atopic dermatitis, rosacea) confirm measurable reductions in inflammatory markers and symptom scores. It is considered one of the few omega-6 fatty acids with a predominantly anti-inflammatory metabolic profile.
Gamma-linolenic acid (GLA), the active component of evening primrose and borage oils, has been studied for atopic dermatitis based on the theory of impaired delta-6-desaturase activity in AD patients. Clinical trial results are mixed, with modest improvements in some studies but no significant benefit in others.
GLA is an omega-6 fatty acid and precursor to prostaglandin E1 (PGE1), a key molecule for tear production and lacrimal gland secretion. Multiple RCTs using GLA combined with EPA/DHA showed improved tear film lipid layer stability, reduced tear evaporation, and reduced DED inflammation. Sources include borage and evening primrose oil.
GLA is an omega-6 fatty acid from evening primrose, borage, and blackcurrant oils that restores skin barrier lipids impaired by delta-6-desaturase deficiency in dry/atopic skin. Clinical studies confirm GLA plasma levels correlate with dry skin improvement, and supplementation reduces TEWL and inflammatory barrier dysfunction. GLA converts to DGLA, producing anti-inflammatory prostaglandins that support skin hydration.
Gamma-linolenic acid (GLA) is the key active constituent in evening primrose oil and borage oil, mechanistically relevant to atopic eczema via the delta-6-desaturase deficiency hypothesis. Some RCTs show improvements in skin hydration and inflammation in atopic dermatitis, though results across trials are inconsistent and the Cochrane review found no consistent benefit.
GLA has demonstrated several cardioprotective properties in human trials including reduction in triglycerides, LDL-cholesterol, platelet aggregation, thromboxane B2, and blood pressure, alongside increases in HDL-cholesterol and prostacyclin production. These lipid and platelet effects collectively reduce cardiovascular risk markers.
GLA (via evening primrose oil) has been tested in multiple RCTs for menopausal hot flashes with some evidence of benefit. A randomized double-blind trial (n=56 menopausal women, BMJ 1994) found gamolenic acid from EPO significantly reduced daytime hot flush frequency. Subsequent trials and systematic review data support a modest but real effect on hot flush severity and frequency.
GLA-containing oils (evening primrose oil) have clinical evidence for relieving several menopausal symptoms including hot flashes, night sweats, and psychological symptoms. Multiple controlled trials support modest but statistically significant benefits. GLA's eicosanoid-modulating effects are hypothesized to underlie these benefits.
GLA influences prostaglandin metabolism through DGLA/PGE1, with PGE1 known to relax smooth muscle and oppose the uterine-contracting prostaglandins central to menstrual pain. A double-blind RCT found GLA supplementation significantly reduced PMS symptom severity in women with documented lower DGLA levels. EPO has a traditional and evidence-based history of use for menstrual symptoms.
GLA has been used for metabolic syndrome (Syndrome-X) based on its documented effects on multiple metabolic syndrome components: triglycerides, HDL-cholesterol, LDL-cholesterol, and blood pressure. Clinical reference sources list metabolic syndrome as a recognized indication for GLA, and its lipid and anti-inflammatory effects are mechanistically relevant.
GLA and its metabolites are required for normal neuronal membrane structure, nerve blood flow, and impulse conduction. Diabetics have impaired GLA synthesis and develop neuropathy partly due to GLA deficiency. Multiple controlled trials show GLA supplementation significantly improves neurophysiological parameters in diabetic neuropathy.
Gamma-linolenic acid (GLA) is an omega-6 fatty acid whose supplementation has been shown in multiple RCTs to benefit diabetic peripheral neuropathy by correcting a metabolic deficiency in GLA conversion seen in diabetic patients. A GLA Multicenter Trial Group RCT (n=111, 12 months) showed significant improvement across 16 neuropathy measures. A 2019 noninferiority RCT demonstrated GLA was comparable to alpha-lipoic acid for painful diabetic neuropathy.
GLA combined with EPA supplementation has been shown in a pilot RCT to preserve and modestly increase bone mineral density in elderly women, supporting a role in osteoporosis prevention. Animal data consistently show GLA enhances calcium absorption and deposition. Evidence is preliminary but mechanistically grounded.
Gamma-linolenic acid (GLA), an omega-6 fatty acid predominant in evening primrose oil and borage oil, has been studied as an active component for perimenopausal hot flash relief via prostaglandin pathway modulation. It is the key bioactive constituent underlying evening primrose oil's studied benefits during perimenopause.
GLA has been investigated for psoriasis both topically and orally, with some evidence supporting modest benefit through its anti-inflammatory eicosanoid-modulating properties. Clinical and mechanistic data suggest GLA may reduce inflammatory components of psoriatic skin, though a systematic review found EPO did not demonstrate effectiveness for psoriasis in controlled trials. Evidence is mixed.
GLA (gamma-linolenic acid), the bioactive in evening primrose and borage oils, is identified in a 2025 PMC systematic review as effective in atopic dermatitis-related itching and inflammatory skin rashes. It suppresses pro-inflammatory arachidonic acid-derived eicosanoid synthesis and has been studied in multiple skin-condition RCTs.
GLA, an omega-6 fatty acid found in evening primrose oil, was studied in a double-blind placebo-controlled trial (Belch et al., 1985, PMID 4082084) where 12 capsules/day of evening primrose oil for 8 weeks resulted in significantly fewer Raynaud's attacks and improved severity scores versus placebo. GLA stimulates endogenous PGE1 production, promoting vasodilation and inhibiting platelet aggregation. Peer-reviewed reviews and Scleroderma & Raynaud's UK cite GLA (~320 mg/day) as one of few dietary components with documented evidence for Raynaud's.
GLA from evening primrose, borage, or blackcurrant seed oil is supported by a Cochrane review of 7 RCTs for RA, showing reduced pain intensity and improved disability versus placebo. GLA is metabolized to DGLA, which competitively inhibits arachidonic acid pathways and directly suppresses T lymphocytes.
GLA supplementation reduces transepidermal water loss (TEWL) and improves skin hydration and barrier function, which are key determinants of skin aging appearance. Clinical trials in adults with dry skin show statistically significant TEWL improvements with GLA. Anti-inflammatory metabolites of GLA also reduce UV-associated skin damage, indirectly protecting against photoaging.
GLA supports skin elasticity by maintaining barrier function, reducing TEWL, and modulating inflammatory pathways that degrade extracellular matrix proteins including collagen. Experimental evidence shows GLA-containing oils restore UV-reduced collagen content in skin models. Clinical improvements in skin barrier function, hydration, and elasticity are documented in human trials.
Clinical trials have found GLA supplementation can significantly lower plasma triglyceride levels. A 4-month study in 12 hyperlipidemic patients receiving 3 g/day of GLA-enriched linoleic/GLA oil showed a 48% reduction in plasma triglycerides (p<0.001). Two small trials in 31 people also showed GLA lowered triglycerides, LDL, and total cholesterol.
GLA is traditionally used and commercially marketed for depression, including postpartum depression, based on its role in eicosanoid regulation and membrane phospholipid composition important for neurotransmission. However, direct clinical evidence from well-controlled trials is limited, and it is primarily listed as a condition for which GLA is 'used' without strong RCT support.
Gamma-linolenic acid (GLA) is an omega-6 fatty acid found in borage oil, evening primrose oil, and black currant seed oil. It is a precursor to prostaglandin E1, which has hair growth-stimulating properties, and has been used traditionally and in supplement formulations for hair loss. Animal studies and preliminary human data suggest it may reduce androgenetic hair loss.
Gamma-linolenic acid (GLA) is the active omega-6 fatty acid in evening primrose oil proposed to address a GLA deficiency contributing to PMS via prostaglandin E1 deficiency. Clinical RCT evidence via evening primrose oil is mixed to negative in most rigorous trials, though GLA remains widely recommended in complementary medicine for PMS.
Body systems that GLA (gamma linolenic acid) may help support.
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