Flaxseed: A Potential Treatment for Lupus Nephritis.

January 1, 1995 Human Health and Nutrition Data 0 Comments

Flaxseed: A Potential Treatment for Lupus Nephritis.

Year: 1995
Authors: W F Clark, A Parbtani, M W Huff, E Spanner, H de Salis, I Chin-Yee, D J Philbrick, B J Holub.
Publication Name: Kidney Inter.
Publication Details: Volume 48; 475.


Previous research by these investigators showed beneficial effects of ALA and lignans from flaxseed in the MRL/lpr lupus mouse, a model for progressive kidney disease. The authors speculated that flaxseed may have positive effects in lupus nephritis due to the hypolipidemic characteristics of ALA and the fact that lignans are potent platelet activating factor (PAF)-receptor antagonists. PAF is a major participant in the activation and propagation of inflammation and has been found to be elevated in patients and animals with lupus nephritis. The inhibition of PAF in lupus animal models is associated with increased survival and decreased protein loss in the urine (proteinuria). In a study by the authors, a flaxseed diet significantly preserved glomerular filtration rate, reduced proteinuria, lymphoproliferation and mortality in MRL/lpr lupus mice and was more potent than previous observations with fish oil. These results led to the present study in which the effects of three doses of flaxseed were assessed in eight patients. Different amounts of flaxseed were used in order to ascertain a dose which would be well tolerated and which would have significant effects on pathogenic mechanisms involved in lupus nephritis. After a baseline period, the normal diets of the patients were supplemented with 15, 30, and 45 g of flaxseed/day sequentially at four week intervals, followed by a five-week washout period. Disease activity, blood pressure, plasma lipids, rheology, PAF-induced platelet aggregation, renal function, and serum immunology were assessed. The authors reported good compliance of the patients when they were administered 15 and 30 g doses of flaxseed. TC and LDL-C were significantly reduced by 11% and 12%, respectively, with 30 g of flaxseed and by 9% and 10%, respectively, with 45 g doses of flaxseed. Following the five week washout period, TC and LDL-C were 7% and 11% lower, respectively, indicating a prolonged lipid lowering effect of flaxseed. There no changes noted in the levels of serum HDL-C, TG or VLDL. ALA, EPA and the n-3/n-6 ratio were increased in serum PLs. Blood viscosity decreased significantly throughout the study and was still reduced following the washout period. PAF-induced platelet aggregation was inhibited by all doses of flaxseed, an effect due to lignans which produce specific reversible and competitive inhibition of PAF. Renal function, assessed by serum creatinine, creatinine clearance and urinary protein measurements were improved over the short term duration of this study. There was a significant decline in serum creatinine with 30 and 45 g, and a concomitant increase in creatinine clearance with increasing flaxseed dose. Proteinuria was reduced with 30 g and to a lesser extent with 45 g of flaxseed. The authors speculated that the reduction in blood viscosity could potentially contribute to a decrease in glomerular capillary permeability and a consequent reduction in proteinuria. Serum immunology measurements showed that complement C3 was significantly elevated by all three doses of flaxseed. CD11b expression on neutrophils, a measure of C3bi receptors, was significantly reduced with the 30 g dose. The investigators concluded that 30 g of flaxseed/day was well tolerated by the patients and conferred significant benefits in terms of renal function as well as inflammatory and atherogenic mechanisms important in the pathogenesis of lupus nephritis. The marked hypocholesterolemic effects of the flaxseed would reduce both the accelerated vascular disease as well as the renal tissue scarring associated with lupus nephritis. The investigators recommend longer term studies with flaxseed as a potential treatment for lupus nephritis.

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