Gammalinolenic acid + rheumatoid arthritis
Linoleic acid (LA), another omega-6 fatty acid, is found in cooking oils and processed foods and converted to GLA in the body. GLA is then broken down to arachidonic acid (AA) and/or another substance called dihomogamma-liolenic acid (DGLA). AA can also be consumed directly from meat, and GLA is available directly from evening primrose oil (EPO), black currant seed oil, and borage oil. Most of these oils also contain some linoleic acid. The average North American diet provides more than 10 times the necessary amount of linoleic acid and tends to have too much omega-6 fatty acids compared to omega-3 fatty acids, another important class of EFAs. In fact, for optimum health, the ratio of omega-6 to omega-3 fatty acids should be between 1:1 and 4:1. The typical North American and Israeli diets are usually in the range of 11:1 to 30:1. This imbalance contributes to the development of long-term diseases such as heart disease, cancer, asthma, arthritis, and depression as well as, possibly, increased risk of infection. Interestingly, not all omega-6 fatty acids behave the same. Linoleic acid (not to be confused with alpha-linolenic acid, which is in the omega-3 family) and arachidonic acid (AA) tend to be unhealthy because they promote inflammation, thereby increasing the risk of the diseases mentioned when consumed in excess. In contrast, GLA may actually reduce inflammation. Much of the GLA taken from the oils mentioned or as a supplement is not converted to AA, but rather to DGLA. DGLA competes with AA and prevents the negative inflammatory effects that AA would otherwise cause in the body. Having adequate amounts of certain nutrients in the body (including magnesium, zinc, and vitamins C, B3, and B6) helps to promote the conversion of GLA to DGLA rather than AA. It is important to know that many experts feel that the science supporting the use of omega-3 fatty acids to reduce inflammation and prevent diseases is much stronger than the information regarding use of GLA for these purposes. Two important, and most studied, omega-3 fatty acids include eicosopentaenoic acid (EPA) and docosahexaenoic acid (DHA), both found in fish and fish oils.
Some preliminary information indicates that GLA, from EPO, borage oil, or black currant seed oil, may diminish joint pain, swelling, and morning stiffness. GLA may also allow for reduction in the amount of pain medication used by those with rheumatoid arthritis. The studies to date, however, have been small in size. Additional research would be helpful, including testing a proposed theory that using GLA and EPA (an omega-3 fatty acid from fish and fish oil) together would be helpful for rheumatoid arthritis. In the meantime, talk to your doctor about whether using GLA is safe for you and then pay attention, over 1 to 3 months of use, to whether your symptoms get better or not. In terms of borage oil, some researchers theorize that it may not be safe to use with non-steroidal anti-inflammatory drugs (NSAIDs such as ibuprofen, which are commonly used for arthritis). This theory needs to be tested.
GLA supplements are derived from evening primrose oil (EPO) as well as black currant seed and borage seed oils. The GLA supplements are often packaged in oil containing capsules. EPO has been the most researched source of GLA.
Generally, high-quality oil will be certified as organic by a reputable third party, packaged in light-resistant containers, refrigerated, and marked with a freshness date.
For general health, there should be a balance between omega-6 and omega-3 fatty acids; the ratio should be in the range of 1:1 to 4:1; the typical North American diet, however, normally provides ratios from 11:1 to 30:1. • The recommended dosage for rheumatoid arthritis is 1,400 mg per day of GLA or 3,000 mg of EPO.
Omega-6 supplements, including GLA and EPO, should not be used if you have a seizure disorder because there have been reports of these supplements inducing seizures. Borage seed oil, and possibly other sources of GLA, should not be used during pregnancy because they may be harmful to the fetus and induce early labor. Doses of GLA greater than 3,000 mg per day should be avoided because, at that point, production of AA (rather than DGLA) may increase.
If you are currently being treated with any of the following medications, you should not use GLA without first talking to your healthcare provider. GLA may increase the effectiveness of ceftazidime, an antibiotic in a class known as cephalosporins, against a variety of bacterial infections. GLA may increase the effects of anti-cancer treatments, such as doxorubicin, cisplatin, carboplatin, idarubicin, mitoxantrone, tamoxifen, vincristine, and vinblastine. Taking omega-6 fatty acids, such as GLA, during therapy with cyclosporine, a medication used to suppress the immune system after an organ transplant, for example, may increase the immunosuppressive effects of this medication and may protect against kidney damage (a possible side effect from this medication). Theoretically, use of NSAIDs, such as ibuprofen, together with borage oil or other GLA containing supplements may counteract the effects of the supplement. Research in this area is needed to know if this theory is accurate.
Individuals taking a class of medications called phenothiazines (such as chlorpromazine, fluphenazine, perphenazine, promazine, and thioridazine) to treat schizophrenia should not take EPO because it may interact with these medications and increase the risk of seizures. The same may be true for other GLA containing supplements.
Arthritis Rheum. 1996 Nov;39(11):1808-17. gamma-Linolenic acid treatment of rheumatoid arthritis. A randomized, placebo-controlled trial.
Zurier RB, Rossetti RG, Jacobson EW, DeMarco DM, Liu NY, Temming JE, White BM, Laposata M.
University of Massachusetts Medical Center, Worcester 01655-0335, USA.
OBJECTIVE: To assess the clinical efficacy and adverse effects of gamma-linolenic acid (GLA), a plant seed oil-derived unsaturated fatty acid that suppresses inflammation and joint tissue injury in animal models, in the treatment of active rheumatoid arthritis (RA). METHODS: 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 gm/day of GLA as the free fatty acid or with sunflower seed oil (placebo) administered in identical capsules. RESULTS: 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). During the second 6 months, both groups exhibited improvement in disease activity. Thus, patients taking GLA during the entire study showed progressive improvement during the second 6 months. In this group, 16 of 21 patients showed meaningful improvement at 12 months compared with study entry. CONCLUSION: GLA at doses used in this study is 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, and should not be viewed as therapy for any disease. Further controlled studies of its in RA are warranted.
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