Borago officinalis: the most important herbal source of GLA

Author: Silvia Leardi
Date: 26/01/2015



Borago officinalis, commonly know as borage or starflower, is an annual herb native to west Mediterranean areas (North Africa, Spain), and naturalized in many other locations. Traditionally this plant was cultivated for culinary and medicinal uses, although today commercial cultivation is mainly as an oilseed which contains γ-linolenic acid (GLA) and other fatty acids.
This report presents the description of the species, its chemical constituents and the rationale for borage oil supplementation in two chronic inflammatory diseases: rheumatoid arthritis and atopic dermatitis.

Botanical description

Fig. 1: Borago officinalis

Fig. 2: Borago officinalis


Kingdom: Plantae
Division: Magnoliophyta
Class: Magnoliopsida
Order: Lamiales
Family: Boraginaceae
Genus: Borago
Species: Borago officinalis L.

Borago officinalis is an hispid annual herb, which height ranges between 20 to 70 cm. Stems are erect, robust, and often branched. Basal leaves are ovate or lanceolate, petiolate; upper leaves are sessile and amplexicaul. Both stems and leaves are bristly and hairy. Bright blue to pink, star-shaped flowers appear in loose racemes during the summer. The fruit of borage is a dark brown or black oval nutlet with a flat base about 2mm x 4 mm in size. Borage has a salty flavor with a cucumbers aroma.

Fig. 3: Borage seeds


Fig. 4: Borage seed

The chemical composition, botanical characteristic and biological activities of Borago officinalis: a review. 2014

Medical toxicology of natural substances : foods, fungi, medicinal herbs, plants, and venomous animals - chapter 50, Borage

Chemical compounds

The whole plant of borage – stem, leaves, flowers and seeds – is a source of essential fatty acids (EFAs), but their quality and amount available in the seed oil are richer.

Fatty acids, triglyceride and tocopherol composition of borage seed oil.

Fatty acid%
Palmitic acid (C16:0)10.7
γ -Linolenic acid (C18:3)21.1
Stearic acid (C18:0)6.4
Eicosenoic acid (C20:1)4.2
Oleic acid (C18:1)18.5
Erucic acid (C22:1)2.3
Linoleic acid (C18:2)36.6
Triglyceride (1)%

Tocopherol mg/kg
γ-tocopherol 39
δ-tocopherol 1320
(1)(P = palmitic, S = stearic, O = oleic, L = linoleic, Ln = gamma-linolenic, E = eicosenoic)

Borage oil is important since it contains the highest amount of γ-linolenic acid (GLA, 18:3 ω-6), which is used as dietary supplement to treat some diseases resulted from its lack in human.
GLA is an ω-6 fatty acid, synthesized just by a few plant varieties. Evening primrose ( Oenothera biennis) and black currant ( Ribes nigrum) oils are well known herbal sources of GLA, but the higher GLA content has been estimated in borage seed oil, as it normally constitutes 15-24% of the oil.

Fig. 5: GLA, 2D structure

Fig. 6: GLA, 3D structure

Other fatty acids available in seed oil are linoleic acid (LA), oleic acid, palmitic acid, stearic acid, eicosenoic acid, stearidonic acid (SDA) and alfa-linolenic acid (ALA). SDA is a precursor for prostaglandin synthesis which is found a little in borage seed oil, while is second frequent fatty acid in leaves (next to ALA). Linolenic acid and palmetic acid are also collected from flowers. The profile of the fatty acids changes upon growth stages.
Antioxidants properties of borage extracts were reported. These properties are attributed to phenolic compounds available in extract of borage seeds, such as rosmarinic acid (the main component of rosemary).
Tocopherols (vitamin E) are also natural effective anti-oxidants and borage species contains high amount of δ-tocopherols.

The chemical composition, botanical characteristic and biological activities of Borago officinalis: a review. 2014

Pathways of GLA metabolism and eicosanoid formation

In normal fatty acid metabolism, γ-linolenic acid is produced as the enzyme Δ6-desaturase metabolite of linoleic acid; GLA is readily converted to dihomo-γ-linolenic acid (DGLA) by the elongase enzyme and then to arachidonic acid (AA).
Prostaglandins (PGs), leukotrienes (LTs) and thromboxanes (TXs) are higly active physiological eicosanoid compounds, that modulate inflammatory, immunologic and proliferative responses. Arachidonic acid is the precursor of the 2-series PGs and the 4-series LTs, whereas dihomo-γ-linolenic acid leads to the formation of the 1-series PGs.


Fig. 7: Metabolism of essential fatty acids to leukotrienes (LTs), prostaglandins (PGs), and thromboxanes (TXs)

A diet rich in borage oil - due to its high GLA content - elevates DGLA concentrations, thereby resulting in an increase in PG1s, e.g. PGE1. In common with all prostaglandins, PGE1 can induce the typical signs of inflammation: redness, edema, pain, heat, and loss of function. In contrast, however, the action of PGE1 on the inflammatory cells, such as the polymorphonuclear leukocytes (PMN), is mainly inhibitory. PGE1 increases intracellular second messenger cAMP (cyclic adenosine monophosphate) and it is this increase in cAMP that reduces the release of lysosomal enzymes, reduces PMN chemotaxis and the margination and adherence of leukocytes in the blood vessels. Similarly, the effect of PGE1 on lymphocytes is believed to be inhibitory. Therefore it has been suggested that PGE1 has a negative feedback role in chronic inflammation, initially aiding in the development of the signs of inflammation but later suppressing inflammation.

Fig. 8: Pathways of ω-6 essential fatty acid metabolism

An additional benefit of a diet rich in γ-linolenic acid is the inhibitory effect on LTs synthesis. LTB4 is one of the major metabolic products of arachidonic acid metabolism and activates the leukocytes responsible for chemokinesis, chemotaxis, adherence, and granulation. DGLA can form a 15-hydroxyl derivative (15-HETrE, 15-hydroxyoctadecadienoic acid) that blocks the transformation of arachidonic acid to leukotrienes. Thus, this is a further way to suppress inflammation through increased intake of GLA.

Status epilepticus associated with borage oil ingestion. 2011

Evening primrose oil and borage oil in rheumatologic conditions. 2000

Borage oil, prostaglandins, TNF-α and rheumatoid arthritis

Rheumatoid arthritis (RA) is a chronic, inflammatory autoimmune disease primarily affecting the synovial tissues of the joint. RA synovitis is characterised by a marked leucocyte infiltration driven in part by local dysregulated production of many proinflammatory cytokines, which promote erosion of cartilage and bone. In particular, tumour necrosis factor-α (TNF-α) has been shown to be a central tissue destructive mediator in RA, promoting (1) cytokine and chemokine production within the RA joint, (2) cellular activation and (3) articular destruction. Conversely the production of anti-inflammatory cytokines (eg, IL-10) increase insufficiently.
The validation of TNF-α as a therapeutic target in RA has encouraged the investigation of signalling pathways regulating its production by cells relevant to the pathophysiology of this disease.
It has been highlighted the presence of two opposing, pathophysiologic, intracellular chains of events engaged consequently to an increase in TNF in the systemic circulation or in a tissue microenvironment, such as an inflammatory lesion. The two chains are identified as “amplification” and “attenuation” cycles.

Fig. 9: Amplification and attenuation feedback cycles

The amplifying, positive feed back cycle tends to result in yet more TNF synthesis and extracellular release. Exposure to TNF causes increases in intracellular phosphodiesterase 4 (PDE4) activity: phosphodiesterase enzyme is primarily responsible for cAMP hydrolysis and degradation. Lowering cAMP tends to increase TNF synthesis, completing the amplification cycle.
Conversely, the attenuating negative feed back cycle elicits decreases in TNF synthesis and release.
Increases of TNF levels induce cyclooxygenase-2 (COX-2) enzyme: COX-2 catalyses a rate-limiting step in the synthesis of prostaglandin H, an intermediate from which all other prostaglandins are generated (Fig.^). When COX-2 levels increase, prostaglandins E series (PGE) increase too.
PGE elevates cAMP, though how it does so is less clear, but probably by allosteric change of adenylate cyclase. Any PGE-mediated cAMP increase tends to lower TNF levels. The precise mechanism by which cAMP levels inversely control TNF-α is unknown, but preliminary evidence points to action at the level of transcriptional control of the TNF-α gene.
Therefore the rationale for borage oil or GLA supplementation in rheumatoid arthritis may consist in PGE-mediated cAMP increase. The cAMP/protein kinase A (PKA) pathway plays a role in control of TNF-α synthesis: while cAMP lowering agents reliably elevate TNF-α levels, PGE raising downregulates tumor necrosis factor output.

Another potential mechanism whereby GLA and DGLA mediate their beneficial effects is through the fibrinolytic process. Fibrin is deposited in excess in rheumatoid joints and it has been shown that the fibrinolytic process is inhibited in rheumatoid arthritis. In a group of subjects with Raynaud phenomenon secondary to rheumatologic conditions, a 12 week supplementation with GLA enhanced fibrinolysis through an increase in tissue-type plasminogen activator, resulting in an increased amount of fibrin degradation products in the blood.

GLA are occasionally used to treat RA. There is moderate evidence that oils containing GLA (borage, evening primrose, or blackcurrant seed oil) afford some benefit in relieving symptoms for RA. A small but clinically meaningful and statistically significant reduction in the signs and symptoms of rheumatoid arthritis disease activity by daily oral supplementation of GLA were documented. However, this use is currently considered “peripheral”. Beyond 3–4 months is required for therapeutic benefits to become apparent.

Phosphodiesterase 4 (PDE4) regulation of proinflammatory cytokine and chemokine release from rheumatoid synovial membrane. 2011

Tumor necrosis factor has positive and negative self regulatory feed back cycles centered around cAMP. 2000

Borage oil reduction of rheumatoid arthritis activity may be mediated by increased cAMP that suppresses tumor necrosis factor-alpha. 2001

Evening primrose oil and borage oil in rheumatologic conditions. 2000

Borage oil supplementation in atopic dermatitis

Atopic dermatitis (atopic eczema, AD) is a chronically relapsing inflammatory, non-contagious and pruritic skin disease, which affects up to 15–20% of children in developed countries. When severe, it can be functionally and socially disabling. The condition improves or resolves with age in most patients.
The pathogenesis is multifactorial and involves environmental, immunological, and genetic factors. It is associated with hyperreactivity to environmental triggers. Atopic dermatitis is strongly linked to a family history of atopy, and often co-occurs with other atopic diseases such as hay fever, asthma and conjunctivitis.
Both epidermal barrier defects and aberrant immune responses are believed to play a pivotal role in the pathophysiology of AD, driving cutaneous inflammation. Skin barrier defects lead to increased transepidermal water loss and increased permeability to irritants and allergens. Epicutaneous antigens encounter Langerhans and dermal dendritic cells that activate Th2 cells.


Fig. 10: The pathogenesis of atopic dermatitis (AD)

Which are the epidermal barrier defects?
Multiple studies emphasize that lesional and even normal appearing skin of AD patients are deficient in various lipids and many keratinocyte structural proteins (filaggrin and loricrin among others) that play important functions. Ceramide levels are lower in atopic eczema compared with healthy skin; furthermore, because of the expression of genes encoding polyunsaturated fatty acid (PUFA) processing enzymes - such as Δ-6-desaturse – is decresead, significantly higher levels of linoleic acid and significantly lower levels of its downstream metabolites GLA, DGLA and arachidonic acid are present in the skin of atopic dermatitis.
In animal cells PUFAs and their products, particularly those of the ω-6 series, are very important since they are key factors in cell membrane fluidity and flexibility, affect activity of membrane-associated proteins (such as receptors and enzymes) and maintain the structural integrity of the skin avoiding transepidermal water loss. Human body skin cannot biosynthesize GLA from linolenic acid, so it must be supplied by diet. Daily consumption of borage seed oil due to its high GLA amount may potentially improve skin dryness and itch.

Most studies showed borage oil is well tolerated, but its use produces only a small degree of benefit. It is likely that there could be multiple defects in the lipid, protein, and gene expression profiles in atopic dermatitis; hence, use of the γ-linolenic acid-rich borage oil may benefit only the small subset of patients with this disease who have a specific γ-linolenic acid formation defect.

Borage oil in the treatment of atopic dermatitis. 2010

Polyunsaturated fatty acids and atopic dermatitis. 2010

New era of biologic therapeutics in atopic dermatitis. 2013


Fig. 1: Borago officinalis
Fig. 2: Borago officinalis. Plate
Fig. 3: Borage seeds
Fig. 4: Borage seed
Fig. 5 e 6: gamma-Linolenic acid; GAMOLENIC ACID; (6Z,9Z,12Z)-octadeca-6,9,12-trienoic acid ...
Fig. 7: Evening primrose oil and borage oil in rheumatologic conditions. 2000
Fig. 8: Borage oil in the treatment of atopic dermatitis. 2010
Fig. 9: Borage oil reduction of rheumatoid arthritis activity may be mediated by increased cAMP that suppresses tumor necrosis factor-alpha. 2001
Fig. 10: The pathogenesis of atopic dermatitis (AD): New era of biologic therapeutics in atopic dermatitis. 2013

Tab. 1: Protective effect of borage seed oil and gamma linolenic acid on DNA: in vivo and in vitro studies. 2013

Silvia Leardi

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