Research Review By Novella Martinello©

Date Posted:

April 2010

Study Title:

Experimental and clinical research findings on the cardiovascular benefits of consuming flaxseed


Bassett CMC, Rodriguez-Leyva D & Pierce GN

Author's Affiliations:

Institute of Cardiovascular Sciences, St Boniface Hospital Research Centre and Department of Physiology, Faculties of Medicine and Pharmacy, University of Manitoba; Cardiovascular Research Division, V.I. Lenin University Hospital, Holguin, Cuba.

Publication Information:

Applied Physiology, Nutrition, and Metabolism 2009; 34: 965-974.

Background Information:

Certain dietary choices can significantly improve cardiovascular health – one of which is regularly including sources omega-3 (?-3) polyunsaturated fatty acids (PUFAs). These can help protect against hypertension, platelet aggregation, dyslipidemia, atherosclerosis, and arrhythmias (1). Flaxseed has been identified as a source of ?-3 PUFAs. It is the richest plant source of the ?-3 PUFA ?-linolenic acid (ALA; C18:3n-3). Flaxseed is also a good source of 2 other nutrients that contribute to positive cardiovascular effects: dietary fibre and phytoestrogens called lignans.

There are 4 forms of flaxseed: whole seed, ground seed, partially defatted flaxseed meal, and flaxseed oil. The seed coat of flaxseed contains the highest known source of lignan phytoestrogens. Flaxseed oil does not contain any dietary fibre or lignans, whereas partially defatted flaxseed meal is rich in fibre and lignans and poor in ALA content. Different forms of flaxseed have shown protective effects against coronary heart disease (CHD) in both clinical and animal data.

This symposium presents the effects of consuming flaxseed in the categories of “animal data” and “clinical data”.



Effects on plasma lipids and atherosclerosis:

Dietary flaxseed can significantly prevent atherosclerotic development under various conditions and has done so in multiple animal models. In general, studies using whole ground flaxseed (0.4 g/day), low ALA partially defatted flaxseed meal (7.5 g/day), or the lignan SDG (40 mg/day) as the dietary treatment report an overall reduction in total cholesterol (TC) levels, and thus a decrease in atherosclerosis, after 4 to 24 weeks of intervention (2-4).

However, flaxseed oil has not been shown to have an effect on plasma lipids and atherosclerosis after 8 weeks of intervention. There may be three reasons for flaxseed’s antiatherogenic effects. First, the antioxidative effects of the lignans within flaxseed may contribute to its antiatherogenic effect. Second, the ?-3 fatty acid content of the flaxseed may provide an anti-inflammatory action that could inhibit atherogenesis. Third, dietary flaxseed may inhibit cell proliferation, an important atherogenic process.

Vascular function:

A diet supplemented with 10% to 20% (caloric intake) of flaxseed protected against the loss of endothelial dependent vascular relaxation induced by cholesterol feeding or hypertensive conditions after 10 to 24 weeks of treatment. Flaxseed had no effect on endothelial-independent routes of modulating vascular response (5, 6).


A diet containing 10% flaxseed supplemented for 16 weeks completely suppressed the incidence of ventricular fibrillation (VF) normally observed during ischemia, and significantly reduced the incidence of VF during reperfusion in hearts obtained from cholesterol fed rabbits (7).


Hypolipidemic effects:

The majority of the studies show that flaxseed slightly reduces TC and LDL levels in normolipidemic (8) and hypercholesterolemic patients (9) and has less impact on high-density lipoprotein (HDL) cholesterol and TG levels in treatments that last from 4 to 24 weeks. Ground flaxseed (38–40 g/day) also reduces the levels of other atherogenic lipoproteins including Lp(a) and apolipoproteins A-1 and B after 12 weeks of dietary intervention. However, results have been mixed. The variable effects of whole ground flaxseed on plasma TC and LDL cholesterol levels are not always related to the dose of flaxseed provided (15–50 g/day) or to general patient characteristics, such as age, sex, or circulating lipid status.

The only 2 studies reporting an effect on plasma lipids demonstrated that flaxseed oil (5.2–20 g/day) may cause more harm than good by increasing circulating TC and decreasing HDL cholesterol levels after 4 to 26 weeks of intervention. The lignan and/or fibre content of flaxseed appears to contribute to the hypolipidemic effect of flaxseed. It is doubtful that the ALA in flaxseed oil has any hypolipidemic action in humans but investigation has only recently begun and is limited.

Anti-inflammatory effects:

Inflammation is a causative mechanism in atherosclerosis. Three studies report anti-inflammatory effects of either flaxseed oil (13.7 g/day or 2 g of ALA from flaxseed oil) or SDG lignan (500 mg/day) in healthy adults after 4 to 12 weeks of dietary intervention and in obese adults consuming 30 g of flaxseed flour a day.

Anti-platelet effects:

The effects of flaxseed on platelet aggregation are controversial. Only 2 trials report that dietary flaxseed provides protection against platelet aggregation. Larger and more recent studies do not find that flaxseed provides any protection against platelet aggregation after 12 weeks to 12 months of treatment (10).

Hypotensive effects:

A large, 12-month study in healthy postmenopausal women reported a significant reduction in both systolic and diastolic blood pressure after consuming 40 g of ground flaxseed per day (11). Two groups also reported that consuming flaxseed oil (15–20 g/day) significantly reduced systolic, diastolic, and mean arterial pressure within a shorter time period (4–12 weeks).

Antioxidant effects:

Surprisingly, two trials reported that flaxseed (50 g/day) or flaxseed oil (20 g/day) caused an increase in markers of oxidative stress, including a decrease in serum protein thiol groups, in hyperlipidemic adults (9) and LDL oxidation in obese adults with markers for insulin resistance after 3 to 4 weeks of dietary intervention.

Clinical Application & Conclusions:

Consuming moderate doses of ground flaxseed (1–4 tbsp,1 tbsp = 7 g) per day can modestly reduce circulating TC (6%–11%) and LDL cholesterol (9%–18%) levels, as well as lowering various markers associated with atherosclerotic cardiovascular disease. Dietary flaxseed may also protect against ischemic heart disease by improving vascular relaxation responses and by inhibiting the incidence of VF. It is important to note that much of the data is still inconsistent, and further research – larger clinical trials such as RCTs – are needed in all areas.

Additional References:

  1. Breslow, J.L. 2006. n-3 fatty acids and cardiovascular disease. Am J Clin Nutr 83(6 Suppl): 1477S–1482S.
  2. Prasad, K., Mantha, S.V., Muir, A.D., and Westcott, N.D. 1998. Reduction of hypercholesterolemic atherosclerosis by CDCflaxseed with very low alpha-linolenic acid. Atherosclerosis, 136(2): 367–375.
  3. Prasad, K. 2005. Hypocholesterolemic and antiatherosclerotic effect of flax lignan complex isolated from flaxseed. Atherosclerosis, 179(2): 269–275.
  4. Dupasquier, C.M., Dibrov, E., Kneesh, A.L., Cheung, P.K., Lee, K.G., Alexander, H.K., et al. 2007. Dietary flaxseed inhibits atherosclerosis in the LDL receptor-deficient mouse in part through antiproliferative and anti-inflammatory actions. Am. J. Physiol. Heart Circ. Physiol. 293(4): H2394–H2402.
  5. Talom, R.T., Judd, S.A., McIntosh, D.D., and McNeill, J.R. 1999. High flaxseed (linseed) diet restores endothelial function in the mesenteric arterial bed of spontaneously hypertensive rats. Life Sci. 64(16): 1415–1425.
  6. Dupasquier, C.M., Weber, A.M., Ander, B.P., Rampersad, P.P., Steigerwald, S., Wigle, J.T., et al. 2006. Effects of dietary flaxseed on vascular contractile function and atherosclerosis during prolonged hypercholesterolemia in rabbits. Am. J. Physiol. Heart Circ. Physiol. 291(6): H2987–H2996.
  7. Ander, B.P., Weber, A.R., Rampersad, P.P., Gilchrist, J.S., Pierce, G.N., and Lukas, A. 2004. Dietary flaxseed protects against ventricular fibrillation induced by ischemia-reperfusion in normal and hypercholesterolemic rabbits. J. Nutr. 134(12): 3250–3256.
  8. Clark, W.F., Parbtani, A., Huff, M.W., Spanner, E., de Salis, H., Chin-Yee, I., et al. 1995. Flaxseed: a potential treatment for lupus nephritis. Kidney Int. 48(2): 475–480.
  9. Jenkins, D.J., Kendall, C.W., Vidgen, E., Agarwal, S., Rao, A.V., Rosenberg, R.S., et al. 1999. Health aspects of partially defatted flaxseed, including effects on serum lipids, oxidative measures, and ex vivo androgen and progestin activity: a controlled crossover trial. Am. J. Clin. Nutr. 69(3): 395–402.
  10. Austria, J.A., Richard, M.N., Chahine, M.N., Edel, A.L., Malcolmson, L.J., Dupasquier, C.M., and Pierce, G.N. 2008. Bioavailability of alpha-linolenic acid in subjects after ingestion of three different forms of flaxseed. J. Am. Coll. Nutr. 27(2): 214–221.
  11. Dodin, S., Lemay, A., Jacques, H., Le´gare´, F., Forest, J.C., and Maˆsse, B. The effects of flaxseed dietary supplement on lipid profile, bone mineral density, and symptoms in menopausal women: a randomized, double-blind, wheat germ placebo-controlled clinical trial. J Clin Endocrinol Metab 2005; 90(3): 1390–1397.