Studying the health benefits of flaxseed lignans continues to stimulate interest within the research community. Lignans belong to a group of compounds commonly referred to as phytoestrogens (“plant estrogens”). Non-steroidal in nature, lignans have an affinity for estrogen receptors α and β and other cellular receptors (1). Flaxseed is the richest source of the lignan secoisolariciresinol diglucoside (SDG). After ingestion, SDG is converted to secoisolariciresinol, which is further metabolized to the mammalian lignans enter diol and enterolactone. SDG compounds have weak estrogenic or anti-estrogenic effects, antioxidant activity, the ability to induce phase 2 proteins and inhibit the activity of certain enzymes. Lignans have been shown to reduce symptoms of cardiovascular disease and the metabolic syndrome by reducing lipid and glucose concentrations, lowering blood pressure, and decreasing oxidative stress and inflammation (2).
A recent randomized double-blind placebo controlled study design assessed the effects of flaxseed lignan complex supplementation during exercise training on a metabolic syndrome composite score in older adults (3). A total of 100 subjects (> or =50 years) were randomized to receive flaxseed lignan (543 mg/day in a 4050 mg complex) or placebo while completing a 6 month walking program (30-60 min/day, 5-6 days/week). A composite Z score of 6 risk factors for metabolic syndrome (fasting glucose, HDL cholesterol, TAG, abdominal adiposity, blood pressure, and inflammatory cytokines) was calculated at baseline and at 6 months. Men taking placebo increased metabolic syndrome composite Z score, but there were no changes in the other groups. Men taking flaxseed lignan had significantly lower diastolic blood pressure relative to men taking placebo, and men taking placebo showed increased TAG relative to men taking flax lignan.
An interesting study from Japan (4) examined the effects of flaxseed lignan (SDG) intake on hypercholesterolemia and liver disease risk factors in moderately hypercholesterolemic men. Thirty men with total cholesterol levels of 4.65 to 6.21 mmol/L (180-240 mg/dL) were randomly assigned to 3 groups; 2 groups received flaxseed lignan capsules (SDG, 20 or 100 mg/d) and the other received placebo capsules for 12 weeks. Compared to the subjects who received placebo, those who received 100 mg of SDG exhibited a significant reduction in the ratio of low-density lipoprotein/high density lipoprotein cholesterol at baseline and at week 12. These results suggest that daily administration of 100 mg SDG can be effective at reducing blood level of cholesterol and hepatic diseases risk in moderately hypercholesterolemic men.
Flaxseed lignans have been studied for anti-cancer effects since the early 1990’s (5) and were reported to reduce pre-cancerous cellular changes and limit angiogenesis (formation of new blood vessels) and metastasis (spread of cancer cells to new areas of the body). This work showed that flaxseed lignans could reduce the progression of breast and colon cancer. Subsequent investigations showed similar results in prostate, lung, bladder, ovarian, colo-rectal, liver, uterine and cervical tissues. There are several proposed mechanisms for the effects of lignans on cancer. A recent paper posted to flaxresearch.com (6) demonstrated that enterolactone (EL) derived from flaxseed lignans suppressed proliferation, migration and metastasis of breast cancer cells by inhibiting extra cellular matrix (ECM) remodeling. To enhance their own survival, tumor cells can manipulate their microenvironment through remodeling the ECM. This remodelling can enhance breast cancer invasion and metastasis and offers a potential target for therapeutic intervention of breast cancer treatment. Further research is suggested to investigate whether EL may have anti-breast cancer activity through effects on remodelling of the ECM.
In addition to cancer, a strong body of evidence exists to support a role for flaxseed lignans – in particular SDG in reducing diabetic complications. Oxidative stress has been implicated in both type 1 and type 2 diabetes (7). Flaxseed and flax lignan complex have been found to improve glycemic control. Animal models of type I diabetes involving streptozotocin administration or utilizing Bio-Breed diabetic (BBdp) prone rats are associated with oxidative stress. SDG treatment reduced serum glucose levels by 75% in the streptozotocin model of diabetes and by 72% in the BBdp rat model of diabetes. These reductions in the development of diabetes were associated with decreases in oxidative stress measured by serum and pancreatic malondialdehyde (MDA). SDG appears to delay the development of diabetes in Zucker diabetic fatty (ZDF) rat model of type 2 diabetes and this effect was associated with a reduction in serum MDA and glycated haemoglobin A1C. The data suggest that SDG may have potential for reducing the incidence of type 1 diabetes and delaying the development of type 2 diabetes in humans.
Flaxseed-derived lignan supplements have been assessed with regard to effects on glycemic control, lipid profiles and insulin sensitivity in type 2 diabetic patients (8). Seventy-three type 2 diabetic patients with mild hypercholesterolemia were randomized to supplementation with flaxseed-derived lignan capsules (360 mg lignan per day) or placebo for 12 weeks. The lignan supplement significantly improved glycemic control as measured by HbA(1c) (-0.10+/-0.65 % vs. 0.09+/-0.52 %). The lignan supplementation resulted in modest, yet statistically significant improvements in glycemic control in type 2 diabetic patients. The authors suggested further work to explore the efficacy of lignans on type 2 diabetes.
The science supporting a positive role for lignans in human health and disease continues to grow. Flaxresearch.com describes over 200 studies that have assessed the potential health benefits of lignans in humans, with supporting evidence from animal studies, under various health related categories.
References
- Jungbauer A, et al. J Steroid Biochem Mol Biol 2014;139:277-289
- Adolphe JL, et al. Br J Nutr 2010;103:929-938
- Cornish SM et al Appl Physiol Nutr Metab 2009:34
- Fukumitsu S, et al. Nutr Res. 2010 Jul;30(7):441-6.
- Serraino M, Thompson LU. Cancer Lett. 1991 Nov;60(2):135-42.
- Mali AV, et al. Asian Pac J Cancer Prev. 2017 Apr 1;18(4):905-915.
- Prasad K, Dhar A. Curr Pharm Des. 2016;22(2):141-4.
- Pan A, et al. PLoS ONE 2007;2:e1148.