Positive effects of flaxseed consumption on flow-mediated dilation and inflammation – New Research

By Kelley Fitzpatrick

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Cardiovascular diseases (CVD) are one of the most common among non-communicable diseases (1). In recent years, medical research has moved toward almost a unifying theory – of chronic disease as a consequence of low-grade, chronic inflammation. Inflammation is a controlled, ordered process whereby the body responds to infection or injury. Symptoms of inflammation include redness, swelling, heat and pain. Chronic inflammation is linked with age-related diseases such as CHD, obesity, diabetes and cancer. Agents that exert anti-inflammatory actions are likely to be important in both prevention and therapy of a wide range of human diseases and conditions. An increasing amount of research suggests that the consumption of ALA may provide protection against inflammatory diseases by reducing inflammatory eicosanoids and cytokines. Pro-inflammatory eicosanoids such as thromboxane A2 (TXA2) and leukotriene B4 (LTB4) are derived from AA. TXA2 is one of the most potent promoters of platelet aggregation known (2). LTB4 increases the release of reactive oxygen species and cytokines like tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), IL-6 and IL-8.

The potential anti-inflammatory effects of flaxseed have been tested and shown to reduce pro-inflammatory eicosanoids. In a clinical study of healthy men, consumption of 1¾ tbsp of flax oil daily for 4 weeks led to a 30% reduction in the immune cells concentration of TXB2, which is an inactive metabolite of TXA2 (2). Concentrations of the pro-inflammatory cytokines TNF-α and IL-1β in immune cells decreased 26% and 28%, respectively. In 64 patients with chronic obstructive pulmonary disease (COPD), serum and sputum LTB4 levels decreased 32% and 41%, respectively, in those patients who received an ALA-rich nutritional support (1.4% ALA) daily for 24 months compared to those who received a low-ALA nutritional support (0.18% ALA) (3). Serum levels of IL-6 decreased 25% in men who consumed 1 tbsp of flax daily for 12 weeks (4). The serum levels of TNF-α decreased by 43% and the production by immune cells of TNF-α, IL-6 and IL-1β, decreased between 18% and 22% in hypercholesterolemics who consumed a diet rich in ALA compared with the average American diet (5).

During inflammation the liver releases acute-phase proteins such as CRP and serum amyloid A (SAA) in response to acute injury, infection, malignancy, hypersensitivity reactions and trauma. CRP and SAA are markers of systemic inflammation, and are present in the lesions of atherosclerosis. CRP is an independent risk factor for CVD (6). In a U.S. study of 23 adults with high blood cholesterol levels, consuming a high-ALA diet based on walnuts, walnut oil and flax oil resulted in a 75% decrease in CRP levels after 6 weeks (7).

A primary promoter of CVD is endothelial dysfunction and is used as a prognostic predictor for the risk of future cardiovascular events (8). Flow-mediated dilation (FMD) is a non-invasive vascular function test to evaluate endothelial dysfunction and is used as a predictor of the severity of coronary artery disease (CAD) (9). In a meta-analysis, flaxseed reduced hs-CRP levels in participants with a BMI of over 30 kg/m2, while whole flaxseed marginally reduced hs-CRP levels (10). Flaxseed has also been shown to improve endothelial-dependent vasorelaxation (11). In a recent paper published on flaxresearch.com (12), the effect of flaxseed consumption on FMD and inflammatory markers in patients with CAD was assessed. In a randomized controlled parallel trial, 50 patients with CAD of both genders were randomly allocated to 12 weeks consumption of flaxseed (30 g/day) or usual care control. Before and after the intervention, changes in brachial FMD and plasma high-sensitivity C-reactive protein (hs-CRP), interleukine-6 (IL-6), and tumor necrosis factor-α (TNF-α) were measured. Forty-four participants (aged 56.43 ± 8.21 years; BMI 26.65 ± 2.44 kg/m2) completed the study. No significant weight change was observed in either group. Compared to control (n = 23), flaxseed consumption (n = 21) was associated with improved FMD (mean of change from baseline was 5.1 vs -0.55%; p = 0.001 for the flaxseed and control, respectively). When compared to control, flaxseed consumption was associated with reduced inflammatory markers (mean of change from baseline for hs-CRP was -1.18 and -0.3 mg/L, p = 0.003; for IL-6 was -7.65 and -0.77 pg/mL, p = 0.017; for TNF-α was -34.73 and -2.18 pg/mL p = 0.001 in flaxseed and control, respectively).

The changes in FMD had an inverse correlation with the changes in IL-6 and TNF-α. High levels of ALA and lignans may have improved the inflammatory markers of the patients in this study. The results show that flaxseed consumption improves endothelial function in patients with CAD and also attenuate selected markers of inflammation. The authors concluded that the consumption of flaxseed may improve CVD risk via mechanisms that affect vascular function and inflammation.

References

  1. Laslett LJ, Alagona Jr P, Clark Iii BA, Drozda Jr JP, et al. J Am Coll Cardiol. 2012;60(25 SUPPL.):S1–S49.
  2. Caughey, G.E.; E. Mantzioris; R.A. Gibson; L.G. Cleland; M.J. James. Am. J. Clin. Nutr. 1996, 63, 116-22.
  3. Matsuyama, W.; H. Mitsuyama; M. Watanabe; K. et al. Chest. 2005, 128, 3817-27.
  4. Paschos, G.K.; F. Magkos; D.B. Panagiotakos; et al. Eur. J. Clin. Nutr. 2007, 31, 1-6.
  5. Zhao, G.; T.D. Etherton; K.R., Martin; et al. Am. J. Clin. Nutr. 2007, 85, 385 – 391.
  6. Getz, G.S. J. Lipid Res. 2005, 46, 1-10.
  7. Zhao, G.; T.D. Etherton; K.R. Martin; J. et al. J. Nutr. 2004, 134, 2991-2997.
  8. Versari D, Daghini E, Virdis A, Ghiadoni L, Taddei S. Diabetes Care. 2009;32(Suppl 2):S314–21.
  9. Koyoshi R, Miura S, Kumagai N, Shiga Y, et al. Circ J. 2012;76:1469–75.
  10. Ren GY, Chen CY, Chen GC, et al. Nutrients. 2016;8:136.
  11. Dupasquier CM, Weber AM, Ander BP, et al. Am J Physiol Heart Circ Physiol. 2006;291:H2987–96.
  12. Khandouzi N, Zahedmehr A, Mohammadzadeh A, et al. Eur J Clin Nutr. 2018 Aug 20. doi: 10.1038/s41430-018-0268-x.