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Rheumatoid Arthritis

Read on for detailed information about how various oils may help alleviate symptoms of Rheumatoid Arthritis.

Flaxseed Oil
The main rationale for the use of flaxseed oil in rheumatoid arthritis (RA) is that its main constituent, ALA, is a precursor to eicosapentaenoic acid (EPA) and docasahexaenoic acid (DHA), both of which have been effective in the treatment of RA symptomatology (jump:footnote 1:1]) and in reduction of inflammatory markers associated with the rheumatoid arthritis disease state (2, 3, 4). In addition, it has been proposed that ALA may actually compete with linoleic acid (LA) for the enzyme delta-6 desaturase, which converts LA to arachidonic acid (AA). In this way, ALA could reduce production of AA and thus also reduce levels of inflammatory eicosanoid compounds, such as PGE2 and LT-B4, which are derived from AA. In the event of positive findings supporting these hypotheses, ALA/flaxseed oil would represent a far less expensive alternative to fish oil (5).

Currently, there is a limited research concerning the effect of ALA/flaxseed oil in RA. In the one clinical trial undertaken to date, ALA treatment at a dose of 9.6g/day for three months was ineffective in altering either clinical or biochemical outcomes among RA patients. More research is needed in this area.

Evening Primrose Oil
Evening primrose oil (EPO) is concentrated in gamma-linolenic acid (GLA), which is converted in the body into dihomo-gamma-linolenic acid (DGLA), a fatty acid that is the precursor to PGE1, an anti-inflammatory prostaglandin compound. PGE1 may play an important role in rheumatoid arthritis (RA), through a variety of mechanisms including its ability to mediate some immune system responses (6, 7, 8) suppress the growth of synovial cells in rheumatic joints (6), and protect the gastric mucosa (stomach lining) that is irritated by non-steroidal anti-inflammatory (NSAID) medications in RA patients (6).

In three randomized, controlled clinical trials and one open trial of EPO in RA patients, therapeutic effects have been modest or absent. One trial showed a statistically significant reduction in NSAID use and a significant improvement in patient disease assessment after 12 months of EPO treatment, 6g/day, compared with paraffin placebo (8). However, another study at the same dose over 6 months showed no reduction in need for NSAIDs or improvement in patient response, although it did report a transient (over 3 months, but not 6 months) improvement in the duration of morning joint stiffness (9). The uncontrolled study reported a slight decrease in skin inflammatory response over the 3 month study period (7). Apart from this, the four clinical trials reported no positive effects compared to placebo on pain, joint stiffness, grip strength, Ritchie articular index, swollen/tender joints, or medication requirements (7, 8, 9, 10). It must be noted, however, that one of these trials was uncontrolled (7), and that two others used olive oil as a placebo (9, 10). Olive oil has subsequently been shown in some trials to have its own therapeutic effect on RA patients, and as such is not a good choice to be used as a placebo (11). A meta-analysis of all clinical trials of GLA (including borage oil and black currant seed oil in addition to EPO) (12) in RA concluded that the combined results were interesting although insufficient at this time to conclusively draw clinical recommendations. The authors also noted that optimum effects found in the studies analyzed were obtained at GLA doses of at least 1.4g/day.

Borage Oil
Borage oil is concentrated in gamma-linolenic acid (GLA), which is converted in the body into dihomo-gamma-linolenic acid (DGLA), which may have important effects on the immune system parameters involved in the development and progression of rheumatoid arthritis (RA). DGLA is converted into the anti-inflammatory prostaglandin compound, PGE1, which mediates some immune system responses (13, 14, 15), suppresses the growth of synovial cells in rheumatic joints, and may have a protective effect on gastric mucosa (stomach lining) that is irritated by non-steroidal anti-inflammatory (NSAID) medications in RA patients (13). Theoretically, the net result of these effects may be a reduction of inflammation and joint irritation in rheumatoid arthritis (RA).

In human studies involving cells taken from healthy (non-RA) subjects, supplementation with 10g/day borage oil was associated with significant, progressive reductions in T-cell proliferation after a single dose, as well as in longer-term studies, over the course of 11 weeks and 24 weeks (16). In the longer-term studies, T-cell proliferation returned to baseline levels three months after cessation of borage oil treatment. These results are potentially significant because of the major role of T-cells in the RA disease process (16). However, it should be noted that these investigations did not involve actual RA patients, and that the longer-term studies only involved two subjects, one each for the different extended study periods.

Two clinical trials have investigated borage oil treatment in RA. The first of these used a dose of 7.2 g/day over a period of 24 weeks, and reported significant improvements in swollen and tender joints, extent of pain, and global disease assessment by physician (17). No changes were shown in hand grip strength, morning stiffness, or any laboratory tests. The second study used borage oil that had been purified to contain approximately 70% GLA, given at a dose of 4g/day (2.8g/day GLA) over study duration of 12 months (18). Again, there were significant improvements in swollen and tender joints and pain, but no changes in grip strength or laboratory parameters, in treated versus placebo patients. Fourteen out of 22 patients treated with borage oil were judged to have undergone a meaningful clinical improvement over 6 months, compared with 4 out of 19 patients treated with placebo. Borage oil patients continued to improve between 6 and 12 months, and placebo patients who were switched to borage oil treatment showed changes similar to those in the borage oil group. Three months after cessation of treatment, symptoms had exacerbated back towards baseline levels.

The information presented here is for educational purposes only and is not intended as curative or prescriptive advice.

Bibliography
1.James, M. J. and Cleland, L. G. Dietary n-3 fatty acids and therapy for rheumatoid arthritis. Semin Arthritis Rheum 1997; 27(2):85-97.
2.Kremer, J. M., Lawrence, D. A., Petrillo, G. F., Litts, L. L., Mullaly, P. M., Rynes, R. I., Stocker, R. P., Parhami, N., Greenstein, N. S., Fuchs, B. R., and et, a. l. Effects of high-dose fish oil on rheumatoid arthritis after stopping nonsteroidal antiinflammatory drugs. Clinical and immune correlates. Arthritis Rheum 1995; 38(8):1107-14.
3.van der Tempel, H., Tulleken, J. E., Limburg, P. C., Muskiet, F. A., and van Rijswijk, M. H. Effects of fish oil supplementation in rheumatoid arthritis. Ann Rheum Dis 1990; 49(2): 76-80.
4.Espersen, G. T., Grunnet, N., Lervang, H. H., Nielsen, G. L., Thomsen, B. S., Faarvang, K. L., Dyerberg, J., and Ernst, E. Decreased interleukin-1 beta levels in plasma from rheumatoid arthritis patients after dietary supplementation with n-3 polyunsaturated fatty acids. Clin Rheumatol 1992; 11(3):393-5.
5.Nordstrom, D. C., Honkanen, V. E., Nasu, Y., Antila, E., Friman, C., and Konttinen, Y. T. Alpha-linolenic acid in the treatment of rheumatoid arthritis. A double-blind, placebo-controlled and randomized study: flaxseed vs. safflower seed. Rheumatol Int 1995;14(6):231-4.
6. Rothman D, DeLuca P, Zurier RB. Botanical lipids: effects on inflammation, immune responses, and rheumatoid arthritis. Semin Arthritis Rheum 1995;25(2):87-96.
7. Hansen TM, Lerche A, Kassis V, Lorenzen I, Sondergaard J. Treatment of rheumatoid arthritis with prostaglandin E1 precursors cis-linoleic acid and gamma-linolenic acid. Scand J Rheumatol 1983; 12(2):85-8.
8. Belch JJ, Muir A. n-6 and n-3 essential fatty acids in rheumatoid arthritis and other rheumatic conditions. Proc Nutr Soc 1998; 57(4):563-9.
9. Brzeski M, Madhok R, Capell HA. Evening primrose oil in patients with rheumatoid arthritis and side-effects of non-steroidal anti-inflammatory drugs. Br J Rheumatol 1991;30(5):370-2.
10. Jantti J, Seppala E, Vapaatalo H, Isomaki, H. Evening primrose oil and olive oil in treatment of rheumatoid arthritis. Clin Rheumatol1989; 8(2):238-44. 89.
11. Soeken KL, Miller SA, Ernst E. Herbal medicines for the treatment of rheumatoid arthritis: a systematic review. Rheumatology (Oxford) 2003;42(5):652-9.
12. Little C, Parsons T. Herbal therapy for treating rheumatoid arthritis. Cochrane Database Syst Rev 2001;(1):CD002948.
13. Rothman D, DeLuca P, Zurier RB. Botanical lipids: effects on inflammation, immune responses, and rheumatoid arthritis. Semin Arthritis Rheum 1995;25(2):87-96.
14. Hansen TM, Lerche A, Kassis V, Lorenzen I, Sondergaard J. Treatment of rheumatoid arthritis with prostaglandin E1 precursors cis-linoleic acid and gamma-linolenic acid. Scand J Rheumatol 1983; 12(2):85-8.
15. Belch JJ, Muir A. n-6 and n-3 essential fatty acids in rheumatoid arthritis and other rheumatic conditions. Proc Nutr Soc 1998; 57(4):563-9.
16. Rossetti RG, Seiler CM, DeLuca P, Laposata M, Zurier RB. Oral administration of unsaturated fatty acids: effects on human peripheral blood T lymphocyte proliferation. J Leukoc Biol 1997;62(4):438-43.
17. Leventhal LJ, Boyce EG, Zurier RB. Treatment of rheumatoid arthritis with gammalinolenic acid. Ann Intern Med 1993;119(9):867-73.
18. Zurier RB, Rossetti RG, Jacobson EW, DeMarco DM, Liu NY, Temming JE et al. gamma-Linolenic acid treatment of rheumatoid arthritis. A randomized, placebo-controlled trial. Arthritis Rheum 1996;39(11):1808-17.

 
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