GLA, a unique and specialized omega-6 fatty acid, is found only in ultra trace amounts in the diet. GLA can be converted to the anti-inflammatory prostaglandin, PGE1, which supports normal tear secretion. Clinical studies report that GLA reduces symptoms and calms inflammation in people with dry eye and improves symptoms and increases tear production in people undergoing corrective laser procedures . It also reduces symptoms and increases anti-inflammatory prostaglandin levels in those with Sjögren’s syndrome.

Featured interview: John D. Sheppard, MD and Stephen C. Pflugfelder, MD on new developments in dry eye treatment and diagnosis
GLA: A Safe & Effective Anti-Inflammatory Omega-6 Fatty Acid
Inflammation: Friend and Foe
The acute inflammatory response defends against invading microorganisms and damaged cells, and is essential for wound healing & tissue repair. Chronic inflammation, however, damages tissues and can lead to or worsen chronic diseases such as arthritis, heart disease & dry eye syndrome.
GLA as an Anti-Inflammatory Nutrient
A recent review underscores the role of the fatty acid gamma linolenic acid (GLA) in modulating the inflammatory response (1). GLA has gained recognition over the last few decades for its anti-inflammatory and anti-cancer actions. Some key findings from controlled clinical trials include:
• In arthritics, several trials report that GLA reduced inflammation, symptoms, and the requirement for NSAIDs
• In inflammatory dry eye, GLA improved symptoms and reduced inflammation; in PRK patients, GLA relieved symptoms, and increased tear production and clearance; in Sjögren's patients, GLA eased ocular discomfort by reducing inflammation and increasing tear content of PGE1
• In diabetics, GLA improved nerve conduction velocity leading to improved blood flow and reduced tingling of extremities
• In patients with acute lung injury, GLA along with EPA improved gaseous exchange
• In breast cancer patients, GLA improved the effectiveness of tamoxifen, reduced side-effects, and hastened therapeutic response
• In uremic pruiritis, a common problem in hemodialysis patients, topically applied GLA relieved symptoms
Sources & Rationale for Supplementation
Dietary intake of GLA is typically negligible as GLA is present only in trace amounts in some green leafy vegetables and nuts. Supplemental sources include the oils of: borage (Borage officinalis), 20-26% GLA; black currant (Ribes nigrum), 15-18%; and evening primrose (Oenoethera biennis), 8-12%. According to Tufts researchers, black currant seed oil is a preferred source because it contains 13-16% of the omega-3 fatty acid alpha-linolenic as well as GLA. Examining the effects of black currant seed oil (vs. placebo) in healthy elderly subjects, researchers from Tufts found that GLA reduced levels of PGE2 and improved immune function (2).
GLA is produced in the body as an intermediate in the metabolism of linoleic acid (LA). However this reaction is very slow and further restricted by alcohol use, stress, smoking, saturated and trans-fatty acid intake, and deficiencies of magnesium, vitamin B6 and zinc. These factors - as well as hypertension, arthritis, psoriasis and diabetes - impair the activity of delta-6-desaturase, the enzyme that converts linoleic acid to GLA. Administering oral GLA is a means to bypass this often inefficient and rate-limiting step in the metabolism of LA to GLA.
Anti-Inflammatory Mechanism of Action
GLA is rapidly converted to dihomo GLA (DGLA) which is incorporated into cell membrane phospholipids. When released by the action of the enzyme phospholipase A2, DGLA competes with arachidonic acid for the enzymes COX and LOX. Arachidonic acid is the omega-6 found abundantly in meat and dairy, and the precursor to pro-inflammatory eicosinoids like PGE2.
The COX products of DGLA include prostaglandins of series 1 (PGE1) and thromboxane A1. These products exert anti-inflammatory, anti-aggregation and vaso-dilatory actions.
A key LOX product of DGLA, 15-HETrE, inhibits production of leukotriene B4 from inflammatory cells including neutrophils. Some research suggests that DGLA may act directly on T-cells to modulate immune response in diseases such as rheumatoid arthritis.
Anti-Cancer Mechanisms of Action
Pre-clinical research indicates that the anti-cancer properties of GLA include: direct cytotoxic action on cancer cells, anti-angiogenic action in tumor cells, stimulation of apoptosis, gene activation, and the effects of DGLA eicosinoids. Preliminary clinical studies suggest that GLA may have benefit in some cancers. GLA injected directly into tumor cells of patients with advanced glioma significantly reduced tumor mass.
Safety of Supplemental GLA
Supplemental GLA has been safely administered in clinical trials at oral doses of 2.8 grams per day or less, for up to a year (3-5). GLA-rich oils have also been commonly used in the U.S. for over 20 years, with no reports of serious adverse events or effects (6).
Americans, who generally obtain an excess of omega-6 fats through over-consumption of meat, dairy, vegetable cooking oils and shortenings, are advised to consume more omega-3s from fatty fish and nuts. The amount of omega-6 fatty acids present in common doses of GLA-rich oil do not make a significant contribution to overall fat intake - typically about 67 grams daily for a 2000 kcal diet with 30% of calories from fats. Further, black currant seed oil contains a recommended ratio of omega-6 to omega-3 fats.
GLA & EPA: Complementary Actions
One concern related to DGLA, is that it could be further metabolized to arachidonic acid with subsequent pro-inflammatory effects. This is not relevant in inflammatory cells such as neutrophils, since these cells lack enzyme (delta-5-desaturase) activity needed to convert DGLA to arachidonic acid (7). Importantly, inflammatory cells from subjects supplemented with GLA produce significantly less pro-inflammatory leukotriene B4 (8,9) .
In contrast to inflammatory cells, high levels of supplemental GLA have been shown in some but not other studies to elevate serum arachidonic acid levels. Human studies, however, have demonstrated that the addition of fish-derived omega-3 EPA in a balanced ratio to GLA, blocks the activity of delta-5-desaturase and prevents elevations in serum arachidonic acid (10,11).
Co-ingesting similar levels of EPA and GLA increases cellular membrane content of both DGLA and EPA (precursor to anti-inflammatory eicosinoids). In short, this supplementation strategy successfully maintains the anti-inflammatory capacity of GLA and increases serum EPA, without causing accumulation of arachidonic acid.
Flaxseed oil is a concentrated source of omega-3 alpha linolenic acid. However, conversion of this fatty acid to EPA is limited, and further metabolism to DHA is very low or negligible (12). Typically, only 15-40% of alpha linoleic is converted to EPA This may, in part, explain why omega-3 fatty acids from fish or fish-oil supplements, but not alpha-linolenic acid, have been found to benefit cardiovascular disease outcomes in primary- and secondary-prevention studies (13). Thus GLA-enriched oils are more effectively paired with fish oil rather than flaxseed oil to promote the complementary actions of GLA and EPA.
References
1. Kapoor R, et al. Gamma Linolenic Acid: An anti-inflammatory omega-6 fatty acid (Review) Curr Pharm Biotech 7:531-34, 2006.
2. Wu D, et al. Effect of dietary supplementation with black currant seed oil on the immune response of healthy elderly subjects. Am J Clin Nutr 70: 536-543, 1999.
3. van der Merwe, et al. The effect of gamma-linolenic acid, an in vitro cytostatic substance contained in evening primrose oil, on primary liver cancer. A double- blind placebo controlled trial. Prostaglandins Leukot Essent Fatty Acids 40:199-202, 1992.
4. Zurier RB, et al. Gamma-linolenic acid treatment of rheumatoid arthritis. A randomized, placebo-controlled trial. Arthritis Rheum39:1808-17, 1996.
5. Keen H, et al. Treatment of diabetic neuropathy with gamma-linolenic acid. The gamma-Linolenic Acid Multicenter Trial Group. Diabetes Care 16:8-15, 1993.
6. Physicians' Desk Reference for Nutritional Supplements, 1st Edition, ISBN 1-56363-364-7, p. 173.
7. Chilton-Lopez T, et al. Metabolism of GLA in human neutrophils. J Immunol 156:2941-47, 1996.
8. Johnson M, et al. Dietary supplementation with GLA alters fatty acid content and eicosanoid production in healthy humans. J Nutr 127:1435-44, 1997.
9. Ziboh VA, et al. Dose-response effects of dietary GLA-enriched oils on human polymorphonuclear-neutrophil biosynthesis of leukotriene B4. Am J Clin Nutr 55:39-45, 1992.
10. Barham JB, et al. Addition of eicosapentaenoic acid to gamma-linolenic acid-supplemented diets prevents serum arachidonic acid accumulation in humans. J Nutr 130:1925-31, 2000.
11. Laidlaw M, et al. Effects of supplementation with fish oil-derived n-3 fatty acids and gamma-linolenic acid on circulating plasma lipid profiles in women. Am J Clin Nutr 77:37-42, 2003.
12. Burdge G, et al. Alpha linolenic metabolism in adult humans. Eur J Lipid Sci Tech 107:426-39, 205, 2005.
13. Wang C, et al. n-3 Fatty acids from fish or fish-oil supplements, but not alpha-linolenic acid, benefit cardiovascular disease outcomes in primary- and secondary-prevention studies: a systematic review. Am J of Clin Nutr 84:5-17, 2006.
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Contact Lens Wear, Dry Eye & Fatty Acids
Contact Lens Wear Can Lead to Dry Eye
Most people are aware that dry eye is a pervasive problem. Estimated to affect up to 1 in 5 adults, it is the most common condition seen in ophthalmology practices. Lesser known, however, is that dry eye is also the most common complaint among those who wear contact lenses.
In some cases, people who already have existing, marginal dry eye can experience worsening of the condition when they begin to wear contact lenses. For others, the lenses themselves may lead to dry eye symptoms over time.
Disturbing the Tear Film
The tear film that hydrates and lubricates the optical surface of the eye is composed of several layers. There is an oily outer layer which helps prevent the tear fluid from evaporating, and an inner layer of fluid that also contains a mucous-like gel which allows the fluid to spread evenly over the surface. A normal and stable tear film is necessary in order to be a successful contact lens wearer who does not suffer from symptoms of dryness or sensation of grittiness.
When a contact lens is placed in the eye, the lens can alter the normal structure of the tear film and affect its rate of evaporation. Greater evaporation leads to increased osmolarity (saltiness or lower volume of tear fluid) - a good predictor of dry eye (1). Tear osmolarity is often elevated in contact lens wearers, and even more so in those who can't tolerate them.
Microvilli Losses
For those who have been wearing their lenses for many years, there may be another contributing factor. The continual rubbing of the lens across the surface of the cornea may result in some loss of the microscopic hair-like structures called microvilli that exist on the outermost layer of the cornea. The microvilli bind to the mucous-like gel in the tear fluid so that the tear film adheres well to the cornea and maintains a stable, uniform layer on the cornea.
It's believed that the constant movement of the contact lens across the surface of the cornea over years of wear may reduce the microvilli. In turn, this can destabilize the tear film and result in contact lens-induced dry eye. It is also thought that discontinuing lens use temporarily will help restore microvilli.
Strategies for More Successful Lens Wear
Contact lenses are often a good alternative for people who are bothered by the cosmetic appearance of eyeglasses or the limitation to activities that they pose. To have a comfortable experience with contact lenses, it's important to be under the care of an eye care practitioner to ensure that the lens fit and lens materials you currently have are the best possible choice for you.
The type of lens chosen may make a difference in reducing the chance for dry eye. While some research has not shown a difference in tear osmolarity between soft, water-containing lens and the rigid, gas-permeable type of lens, in some cases soft, high-water content lenses may not be the best choice (2). In general, the more water a soft contact lens contains, the more prone it is to become dehydrated. As water evaporates from the front of the water-containing lens during wear, the lens draws moisture from the tear film. In addition to choosing appropriate lens materials, your eye doctor may also recommend lubricating drops or other aids, and suggest ways to modify environmental factors that can exacerbate dry eye such as overheated rooms, use of hairdryers or uninterrupted time at the computer.
Important Fatty Acids Can Be Helpful
An additional strategy is to try supplemental GLA and EPA, fatty acids that can bolster one's own natural, inflammation-fighting ability. Whatever the cause of dry eye - insufficient tear production, evaporation, chronic allergy or other - the result is an inflammatory reaction, and the contact lens wearer with symptoms of dryness is no exception (3). Research suggests that fatty acid supplementation can help calm inflammation and improve dry eye symptoms (4). Balanced amounts of GLA and EPA work together to reduce production of pro-inflammatory compounds while increasing the manufacture of compounds that are anti-inflammatory.
References

1. Tomlinson A, et al. Tear film osmolarity: determination of a referent for dry eye diagnosis. Invest Ophthalmol Vis Sci 47:4309-15, 2006.
   
2. Iskelei G, et al. Comparison of tear-film osmolarity in different types of contact lenses. CLAO J 28:184-6, 2002.
   
3. Kallinikos P, et al. Assessment of stromal keratocytes and tear film inflammatory mediators during extended wear of contact lenses. Cornea 25:1-10, 2006.
   
4. Barabino S, et al. Systemic linoleic and gamma-linolenic acid therapy in dry eye syndrome with an inflammatory component. Cornea 22:97-102, 2003.
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GLA and Vision-Corrective Laser Surgery
Know someone who's scheduled for vision-corrective laser surgery? GLA may help!
LASIK or PRK Can Cause Temporary Dry Eye
Some people, who are appropriate candidates, opt for laser surgery to help correct their vision. The two most common types of procedures are LASIK (Laser In Situ Keratomileusis) and PRK (Photorefractive Keratectomy). These popular procedures use a laser or a combination of microsurgery and laser to reshape the eye's cornea. Reshaping the cornea alters the focusing power of the eye, allowing one to become less dependent upon glasses or contact lenses.
Having Dry Eye Before Surgery May Prolong or Worsen Symptoms Afterward
One common side-effect of the surgery is dry eye. It can make the cornea less sensitive, resulting in lower tear production and inflammation. The good news is that dry eye is temporary, typically lasting no more than a month. But symptoms may last longer and be more severe in people who already have dry eye before they undergo the surgery (1).
What Is Dry Eye Syndrome?
A common condition, dry eye has many causes. One of the most common reasons is the normal aging process. It's also associated with certain conditions such as rosacea and Parkinson's. Women frequently experience dry eye, especially as they enter menopause. Symptoms include itching, burning, or a gritty sensation - even tearing when the eye is irritated. Visual efforts like reading or computer time can aggravate symptoms, and other factors such as hot, dry, or windy climates; high altitudes; air-conditioning; and cigarette smoke are also contributors. Ironically, contact lens wear can also contribute to or worsen dry eye, which often leads people to laser surgery.
Special Fatty Acids May help
Italian researchers recently investigated the effects of fatty acids on dry eye in people undergoing PRK. Thirty patients were given supplements of linoleic acid and gamma-linolenic acid or GLA. Another group underwent PRK without the supplement. Compared to the untreated control patients, the group getting fatty acids were found to have significantly fewer symptoms of dry as measured by questionnaire. They also scored better in the Schirmer test-a method for measuring tear production-and their eyes were able to more readily clear a staining dye from their tears, reflecting better ocular surface sensitivity and tear clearance.
GLA is a specialized fatty acid with the ability to modify inflammation and support tear production (2-4). These researchers concluded that GLA as a precursor to anti-inflammatory compounds, could be helpful in increasing tear production and clearance after PRK (5).
HydroEye is a unique, oral formulation for dry eye relief. It provides GLA and nutrient cofactors that help dampen inflammation and support a healthy tear film.
References

1. Toda I et al. Laser-assisted in situ keratomileusis for patients with dry eye. Arch Opthalmol 120:1024-28, 2002.
2. Aragona P et al. Tear PGE1 levels in dry eye patients after treatment with essential fatty acids. Invest Ophthalmol Vis Sci 42:5259, 2001.
3. Bababino S et al. Efficacy of systemic linoleic and gamma-linolenic acid therapy in dry-eye syndrome with inflammatory component. ARVO Annual Meeting, Fl, May 2002, abstract 2105.
4. Horobin DF et al. Treatment of the sicca syndrome and Sjögren's syndrome with EFA, pyridoxine, and vitamin C. Prog Lipid Res 20:253-4, 1981.
5. Macri A et al. Effect of linoleic acid and gamma-linolenic acid on tear production, tear clearance and on the ocular surface after photorefractive keratectomy. Graefes Arch Clin Exp Ophthalmol (published online, May 27, 2003)
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Oral Omega Fats, GLA & LA, Increase Tear Production After PRK
Introduction:
PRK is known to cause a temporary reduction in corneal sensitivity, leading to tear film changes, lowered reflex tearing, and production of inflammatory cytokines and free radicals. Transitory dry eye is a common complication after PRK and LASIK, lasting longer in patients with preoperative dry eye (1).
The anti-inflammatory properties of the fatty acid GLA have long been known. Recent studies report that oral administration of GLA and LA leads to a significant increase in tear concentrations of anti-inflammatory prostaglandin E1 (2,3), and reduces the symptoms of dry eye (2). The aim of this study was to evaluate the effects of GLA and LA on tear production, tear fluorescein clearance, dry eye symptoms, and the ocular surface after PRK (4).
Methods:
In this randomized, controlled trial, 31 patients received modest amounts of oral GLA and LA 3 days prior to 30 days after undergoing PRK. Another 29 patients underwent PRK without the supplement, serving as controls. The following measurements were made at baseline and at the end of the study period: symptom questionnaire, Schirmer 1 test, fluorescein clearance test using standardized visual scale and corneal fluorescein staining.
Results:
All 60 patients completed the study. Statistical analysis showed a significant mean difference between the groups for dry eye symptoms, fluorscein clearance, and Schirmer's results. Compared to controls, the treated group had lower symptom scores, greater Schirmer test values, and more favorable fluorescein clearance scores [See Figures 1-3]. Both groups showed no signs of corneal staining at baseline. While more areas stained in controls than treated patients at 1 month post-surgery (0.09 ± 0.10 vs. 0.25 ± 0.21 respectively), the difference was not significant. The researchers concluded that oral precursors of prostaglandin E1, GLA and LA, could be helpful in increasing tear production and clearance after PRK.
Figure 1. Results of symptoms questionnaire (mean score) before starting study (T0) and 1 month after PRK (T1). (*P<0.05)

Figure 2. Results of Schirmer 1 test (mm/5 min) before starting study (T0) and 1 month after PRK (T1). (*P<0.0001)

Figure 3. Results of fluorescein clearance test by means of visual scale (mean score) before starting study (T0) and 1 month after PRK (T1). (*P<0.0001)

References

• Toda I et al. Laser-assisted in situ keratomileusis for patients with dry eye. Arch Opthalmol 120:1024-28, 2002.
• Aragona P et al. Tear PGE1 levels in dry eye patients after treatment with essential fatty acids. Invvest Ophthalmol Vis Sci 42:5259, 2001.
• Barabino S et al. Systemic linoleic and gamma-linolenic acid therapy in dry-eye syndrome with inflammatory component. Cornea 22(2): 97–101, 2003.
• Macri A et al. Effect of linoleic acid and gamma-linolenic acid on tear production, tear clearance and on the ocular surface after photorefractive keratectomy. Graefes Arch Clin Exp Ophthalmol (published first online, May 27, 2003) Full paper available upon request.
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Supplemental GLA Improves Dry Eye in Sjögren's Syndrome
Inflammation and Sjögren's Syndrome
Affecting more than 1.4 million Americans, Sjögren's syndrome is an autoimmune disorder in which immune cells attack and destroy the glands that produce tears and saliva. The hallmark symptoms of the disorder are dry mouth and dry eyes. Sjögren's syndrome is also frequently associated with rheumatic disorders such as rheumatoid arthritis.
T-cell infiltration and markers of immune activation have been noted in both the conjunctiva and lacrimal glands of these patients. Topical anti-inflammatory treatment of patients with dry eye reportedly produces a significant reduction of activated lymphocyte in the conjunctiva, thus demonstrating the potential for anti-inflammatory treatment of dry eyes.
Anti-inflammatory Activity of GLA
Gamma-linolenic acid (GLA) and its precursor linoleic acid (LA) are essential fatty acids found in certain plant seed oils such as black currant seed oil. Oral administration of GLA and LA has been shown to have beneficial effects in the treatment of chronic inflammatory disorders such as rheumatoid arthritis, and several pilot studies conducted in the 1980's suggest that these fatty acids may also benefit the ocular status of patients with Sjögren's.
GLA is metabolized to dihomo-linolenic acid (DGLA), the immediate precursor of PGE1, an eicosanoid with known anti-inflammatory action. In addition, both GLA and DGLA modulate the immune responses by acting directly on T lymphocytes. Researchers from the University of Messina in Italy now report that modest amounts of supplemental GLA and LA raise PGE1 tear content in Sjögren's, and improve signs and symptoms of ocular discomfort in these patients.
Design and Methods
This randomized, double-blind, controlled trial involved 40 patients with primary Sjögren's Syndrome divided into 2 groups. One group received GLA (15 mg) and LA (112 mg) twice daily for 1 month (GLA group), while the other group received placebos. Subjects underwent 3 examinations: baseline (T0), after 1 month (T1), and 15 days after treatment was suspended (T2). At each exam, the following tests were performed: tear sampling from the inferior meniscus, TBUT, fluorescein stain of the ocular surface, and tear basal secretion. A symptom score was also obtained each time. PGE1 was evaluated by enzyme immunoassay, and PGE1 content of tears was the primary endpoint.
Results
Tear PGE1 levels were significantly increased in the GLA group after 1 month of treatment. Fifteen days after treatment was halted, a significant reduction of the PGE1 levels toward baseline was observed. The symptom score was significantly lower in the GLA group after 1 month, with several symptoms (burning, foreign body sensation and dryness) remaining improved after treatment was stopped. The corneal fluorescein stain in this group also showed a significant improvement after the first month, which was sustained 15 days after treatment cessation.
No statistically significant differences were found for the other tests. In contrast to the GLA group, no statistically significant changes were noted in the placebo group at all examination time points. These results are summarized in the table below (group 1 = supplemented; group 2 = placebo).


Conclusions
According to the authors, these results indicate that supplemental GLA and LA effectively increases PGE1, an indicator of anti-inflammatory activity, improves ocular surface status and reduces dry eye symptoms.
Reference
Aragona P, et al. Systemic omega-6 essential fatty acid treatment and PGE1 tear content in Sjogren's syndrome patients. Invest Ophthalmol Vis Sci 46:4474-9, 2005.
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Black Currant Seed Oil and EFAs in Dry Eye and Immunity
Studies have shown that dry eye patients experience a chronic inflammatory cycle, causing symptoms and impacting tear production. A Phase III FDA study of cyclosporine, an immunomodulatory drug, demonstrated that in moderate and severe cases of Sjögren's syndrome and keratoconjunctivitis sicca (KCS), markers of inflammation were significantly reduced from baseline following treatment with this drug. However, this potent immunomodulatory drug is not a first-line defense.
A more effective and preventive approach may be to address the biochemical basis of a healthy and intact tear film. Studies have shown that nutritional supplementation with omega-3 and omega-6 fatty acids and nutrient cofactors involved in the biosynthesis of the prostaglandin PGE1 result in reduced symptoms in dry-eye and KCS patients (1,2). PGE1 is necessary for tear secretion and also regulates inflammation. Essentially, in the event of reduction of PGE1 synthesis (due to a deficiency of omega-3 and omega-6 fatty acids), there is overproduction of series 2 prostaglandins (PGE2). Increased PGE1 production is anti-inflammatory because it down-regulates PGE2 production, and thus reduces over-reactive B-cell activity and may be a regulator of the arachidonic acid cascade. Wu and colleagues carried out a placebo-controlled study of the effect of dietary supplementation with black current seed oil (BCSO) on immune response in healthy subjects 65 years or older (3).
Methods:
This was a randomized double-blind study. Forty patients were randomized to receive either 750 mg BCSO or 750 mg soybean oil. BCSO contains linoleic acid and 15% gamma-linolenic acid (GLA) - both omega-6 fatty acids, as well as the omega-3 fatty acids alpha-linolenic acid and stearidonic acid. The ratio of omega-3 to omega-6 fatty acids in BCSO is about 1 to 4. The level of vitamin E intake in both groups was controlled equally. Supplementation continued for 2 months.
Results:
BSCO supplementation, significantly increased plasma concentrations of gamma-linolenic acid (omega-6), alpha-linolenic acid (omega-3), and dihomo-gamma-linolenic acid compared with baseline. These increases were not evident in the control group. The BCSO group exhibited enhanced response to tetanus toxoid. In the BCSO group, stimulated PGE2 production was significantly reduced from baseline (488 ng/L to 258 ng/L). This was significantly (p<0.05) different from the control (soybean oil) group, which did not exhibit this reduction (Figure). The authors concluded that BCSO has a moderate immune enhancing effect attributable to reduction of PGE2 production.


Comment:
This study and previous research suggests that the combination of omega-3 and omega-6 fatty acids in black current seed oil both results in increased PGE1, which both stimulates aqueous tear secretion and reduces the production of PGE2.
ScienceBased Health's HydroEye^® is a proprietary blend of BCSO (rich in both omega-3 and 6 fatty acids), Cod Liver Oil (additional omega-3 fatty acids, Vitamin A, and eicosanoids), Vitamins B6 and C and Magnesium. This optimal ratio of omega-3 and omega-6 fatty acids along with the essential cofactors for the PGE-1 pathway, results in increased PGE1 production. PGE1 both stimulates aqueous tear secretion and reduces inflammation by down-regulating production of PGE2 (enhancing T-cell production and inhibiting over-reactive B-cells).
References

• Horrobin DF, Campbell A, McEwen CG: Treatment of the Sicca Syndrome and the Sjögren's Syndrome with E.F.A., Pyridoxine and Vitamin C. Prog Lipid Res 8(4): 253-4, 1981
• Oxholm P, Manthorpe R, Prause JU, Horrobin D: Patients with Primary Sjögren's Syndrome Treated for 2 Months With Evening Primrose Oil. Scand J Rheumatology 1986; 15:103-108.
• Wu D, Meydani M, Leka L, et. al.: Effect of dietary supplementation with black current seed oil on the immune response of healthy elderly subjects. Am J Clin Nutr 1999;70:536-543.
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Dry Eye: A Clinical Trial of Essential Fatty Acids
In the previous EduFacts we summarized preliminary work by Horrobin and colleagues (1) which indicated that an effective approach to the treatment of dry eye disorders may be to address the biochemical basis of an intact tear film. In this preliminary study the authors had evaluated the use of supplemental intake of the essential fatty acids (EFA); linoleic and gamma linolenic acids; vitamin B6 ; and vitamin C to treat dry eye. These nutrients are necessary components of the pathway for biosynthesis of prostaglandin E1 (PGE1), which is necessary for aqueous tear secretion by the lacrimal glands. The rationale for their study was based on earlier research showing that gamma linolenic acid (GLA), an upstream metabolite of the EFA linoleic acid, was lower among patients with Sjögren's Syndrome. This suggested a breakdown in the biochemical pathway which might be remedied by supplying both GLA, linoleic acid and the vitamin cofactors involved.
Another controlled study of treatment with precursor EFAs was performed by Oxholm and colleagues on patients with primary Sjögren's Syndrome (2).
Methods:
28 patients with primary Sjögren's Syndrome were studied in a "cross-over" clinical study. Each patient received either Efamol (73% cis-linoleic acid, 9% gamma linolenic acid) or placebo for 8 weeks. Dosing was 6 3g capsules daily. Then each patient was "crossed-over" and received the opposite treatment for 8 more weeks. The initial treatment assignment was randomly chosen for each patient and the study was double masked - neither patients nor clinicians knew the treatment given to the patient. Clinical tests for keratoconjunctivitis sicca (KCS) included Schirmer test, tear-break-up-time, and Bijstervald score. These tests were evaluated before and after treatment. A combined ocular score was also computed. In addition the levels of DGLA (a metabolite of linoleic acid produced during biosynthesis of PGE1) were measured in serum and in erythrocytes before and after treatment.
Results:
Statistically significant baseline-to-post-treatment improvement in the overall ocular score was found in the Efamol group (p<0.05). Fewer patients in the control group experienced improvement (baseline-to-post-treatment) in ocular score. Furthermore, levels of the metabolite Di-hommo-gamma linolenic acid (DGLA) were increased significantly in both plasma (25% increase, p<0.001), and erythrocytes (10% increase, p<0.05) during Efamol treatment but not placebo treatment.

References

• Horrobin DF, Campbell A, McEwen CG: Treatment of the Sicca Syndrome and the Sjögren's Syndrome with E.F.A., Pyroxidine and vitamin C. Prog Lipid Res 8(4): 253-4, 1981.
• 2. Oxholm P, Manthorpe R, Prause JU, Horrobin D: Patients with Primary Sjögren's Syndrome Treated for 2 Months With Evening Primrose Oil. Scand J Rheumatology 1986; 15:103-108.
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Amount of GLA (per day) in selected ScienceBased Health products:

Dry Eye Relief

    HydroEye provides:

• GLA: 235 mg