Latin name: Linum usitatissimum
Pharmacopoeial name; Lini semen
Other names; flax, linseed
Flaxseed, one of the oldest cultivated crops, continues to be widely grown for oil, fibre, and food . Flaxseed oil is an excellent source of the omega-3 fatty acid linolenic acid with typical levels of 55% in the oil. Increasing demand for edible oil sources with significant percentages of omega-3 fatty acids is resulting in consumption of flaxseed as a functional food.
Analysis of flaxseed conducted by the Canadian Grain Commission showed the average composition of commercial seed was 41% fat, 20% protein, 28% total dietary fibre, 7.7% moisture, and 3.4% ash (1). Minor components included: cyanogenic glycosides, phytic acid, phenolics, trypsin inhibitor, linatine, lignans (phytoestrogens), minerals, vitamins, cadmium, selenium and cyclolinopeptides (CLs) Flaxseed contains around 20% substantial soluble and 9% insoluble fibre.
The oil is primarily in the form of triacylglycerides of linoleic (17%), oleic (20%), palmitic (6%), and stearic (4%) acids. Minor lipids and lipid soluble compounds include monoacylglycerides, diacylglycerides, tocopherols, sterols sterol-esters, phospholipids, waxes, CLs, free fatty acids (FFAs), carotenoids, chlorophyll, and other compounds. Human metabolic pathways do not synthesize ALA, an essential polyunsaturated fatty acid in flaxseed. It is an intermediate in the biosynthesis of hormone-like eicosanoids, which regulate inflammation and immune function in higher animals (2) and may contribute to effects of dietary flaxseed oil.
There are many flaxseed products that are consumed including: whole seed, ground whole seed, flaxseed oil, partially defatted flaxseed meal (usually from expeller pressing), fully defatted flaxseed meal (from solvent extraction), flaxseed mucilage extracts, flaxseed hulls, flaxseed oleosomes and flaxseed alcohol extracts. Each of these products is associated with specific beneficial health effects. Although each fraction contains more than one bioactive component, reports commonly ignore the presence of a plurality of bioactive compounds in flaxseed fractions or attribute the effect of a component of the flaxseed on the observed effect.
Based on the complexity of the flaxseed fractions used for much of the research discussed above it is not possible to attribute the health benefits of flaxseed consumption to a sole bioactive component present in flaxseed. The exploration of the biological roles of flaxseed polyunsaturated fatty acids and lignans has been substantial in contrast to the modest efforts made on other components (3-8).
Uses of Flaxseed
Inclusion of flaxseed products has also been associated with improvement in blood lipids. Inclusion of 20% flaxseed in diets of rats decreased total plasma cholesterol, triglyceride (TG), and low-density lipoprotein (LDL) cholesterol by 21, 34, and 23%, respectively. Supplementation with 30% flaxseed had a more pronounced effect, reducing the same factors by 33, 67, and 23% (9).
In human studies, 15 g/d of flaxseed administered for three months was associated with reduction in serum TG and LDL cholesterol without any alteration of high-density lipoprotein (HDL) cholesterol (10). It has also been reported that consumption of 50 g flaxseed/day for four weeks lowered the plasma LDL cholesterol by 8% in young healthy adults (11).
A meta-analysis of studies published from January 1990 to October 2008 revealed a consensus regarding the effect of flaxseed products on blood lipids. All flaxseed interventions, included in the analysis, reduced both total cholesterol and LDL cholesterol. While flaxseed oil had no significant effect on either cholesterol or LDL cholesterol, interventions with whole flaxseed and lignan enriched supplements (flaxseed alcoholic extracts) lowered total cholesterol and LDL cholesterol. Female subjects, and individuals with elevated initial cholesterol concentrations, showed a greater response.
These experimental findings support the hypothesis that flaxseed consumption has a positive effect on suppressing the development of atherosclerosis. Recently it was demonstrated that consumption of one whole flaxseed product in the form of a bagel, muffin, bar or bun containing 30 g of flaxseed by a group of patients displaying pulmonary artery disease and elevated blood pressure significantly reduced both systolic and diastolic blood pressure (12). In this study the authors reported significant linear correlations between blood pressure lowering effects and markers of flax consumption. Based on the weight of evidence from human clinical trials available prior to 2011 Health Canada’s Food Directorate concluded that a claim linking consumption of ground whole flaxseed and blood cholesterol lowering was warranted.
Secoisolariciresinol diglucoside is a phytochemical and antioxidant that acts as a precursor of mammalian lignans and a phytoestrogen (13). Consumption of the lignans or the a flaxseed lignan complex FLC is reported to slow the progression of atherosclerosis in humans and other mammals (14) Hypercholesterolemic humans were treated with 300 mg of 600 mg of FLC for eight weeks. The 300 mg dose reduced total cholesterol and LDL cholesterol by 15 and 17%, respectively, without any change in the ratio of total cholesterol/ HDL cholesterol. A higher dose of 600 mg reduced the serum total cholesterol and LDL cholesterol by 24 and 22%, respectively, with a decrease in the total cholesterol/HDL cholesterol ratio.
Authors of a number of studies have suggested that the primary benefit of flaxseed oil consumption is due to its
ALA content. Flaxseed oil consumption exerts several effects on inflammatory mediators and markers depending on dose.
Flaxseed oil given at 14 g/d to human subjects over 4 weeks decreased the levels of tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), and cytokines. A lower dose did not have this effect (15). Supplementation of the diet with 6% ALA depressed the levels of IL-6 and IL-10 and increased the production of TNF-a (16).
Flaxseed protein products are rich in arginine, an amino acid that, when present in the vascular endothelia, can
lower blood pressure (17).
A recent review of flaxseed proteins concluded that the association of flaxseed proteins with mucilage was an advantage in their applications in food formulations. However, mucilage increases the viscosity of aqueous solutions making the separation of protein difficult. It was noted that preparing protein isolates that were free from mucilage was technically difficult due to viscosity (18). Flaxseed protein hydrolysis products may inhibit angiotensin I-converting enzyme but only a few studies have focused on the hydrolysis of flaxseed protein as would occur under gut conditions. Chavali (19) investigated the in vitro digestion of flaxseed protein and found that whole ground flaxseed resisted digestion in both the modelled stomach and intestinal digestion conditions but that treatments that would inactivated flaxseed protease inhibitors or removed mucilage or both increased total digestion. The amount of undigested protein in whole ground seed was just 12%.
Effects of flaxseed mucilage on the digestive tract have been investigated recently in human and animal trials. The products were supplied in solution or incorporated into food. As would be expected for consumption of fibre, feelings of satiety and fullness were expressed by subjects consuming 2.5 g of soluble fibre in contrast to control subjects. A significant decrease in subsequent energy intake was observed after the flaxseed drink compared to the control (2937 vs. 3214 kJ). There was no difference in either appetite ratings or energy intake by subjects that consumed soluble flaxseed fibre in a drink or as a tablet. Consuming flaxseed mucilage liquid three times a day was compared to consuming the same amount in the form of bread (20). Fibre consumed by both means lowered total fasting cholesterol and LDL cholesterol after seven days. Faecal fat excretion increased with both treatments while the liquid form of the mucilage, and not the bread product, increased energy excretion in faeces. The authors concluded that soluble flaxseed fibre might be used to reduce cholesterol and may be useful in controlling energy balance.
The effects of soluble flaxseed fibre on appetite, blood triglycerides and appetite regulating hormones were observed for seven hours after a test meal (21). Higher levels of dietary fibre served with the meal (3.4 g/MJ from flaxseed) were associated with decreased blood triglyceride (18%) after the meal. Additionally, satiety and fullness ratings increased while insulin decreased with the higher dietary fibre treatment. The concentrations of hormones ghrelin, cholecystokinin and glucagon-like peptide 1 were not affected by the treatment.
1. DeClercq, D. R. (2012). Available at: http://www.grainscanada.gc.ca/flax-lin/trend-tendance/qfc-qlceng. htm
2. Mantzioris, E., James, M. J., Gibson, R. A., & Cleland, L. G. (1994). American Journal of Clinical Nutrition, 59, 1304309.
3. Landete, J. M. (2012). Food Research International, 46, 410-424.
4. Lane, K., Derbyshire, E., Li, W., & Brennan, C. (2014). Critical Reviews in Food Science and Nutrition, 54, 5720-579
5. Katare, C., Saxena, S., Agrawal, S., Prasad, G., & Bisen, P. S. (2012) Journal of Nutrition & Food Sciences, 2, 120-128
6. Rodriguez-Leyva, D., Bassett, C. M. C., McCullough, R., & Pierce, G. N. (2010). Canadian Journal of Cardiology, 26, 489-496
7. Rabetafika, H. N., van Remoortel, V., Danthine, S., Paquot, M., & Blecker, C. (2011). International Journal of Food Science and Technology, 46, 221-228
8. Carayol, M., Grosclaude, P., & Delpierre, C. (2010). Cancer Causes & Control, 21, 347-355.
9. Ratnayake, W. M. N., Behrens, W. A., Fischer, P. W. F., (1992) The Journal of Nutritional Biochemistry, 3, 232-240.
10. Bierenbaum, M. L., Reichstein, R., & Watkins, T. R. (1993). Journal of the American College of Nutrition, 12, 501-504.
11. Cunnane, S. C., Hamadeh, M. J., Liede, A. C., Thompson, L. U.,
12. Wolever, T. M., & Jenkins, D. J. (1995). American Journal of Clinical Nutrition, 61, 62-68.
13. Rodriguez-Leyva, D., Weighell, W., Edel, A. L., LaVallee, R.,
14. Dibrov, E., Pinneker, R., et al. (2013). Hypertension, 62, 1081-1089
15. Adolphe, J. L., Whiting, S. J., Juurlink, B. H. J., Thorpe, L. U., &
16. Alcorn, J. (2010). British Journal of Nutrition,103, 929-938.
17. Prasad, K. (2009). Journal of Cardiovascular Pharmacology and Therapeutics, 14, 38-48.
18. Caughey, G. E., Mantzioris, E., Gibson, R. A., Cleland, L. G., & James, M. J. (1996). American Journal of Clinical Nutrition, 63, 116-122.
19. Chavali, S. R., Zhong, W. W., & Forse, R. A. (1998). Leukotrienes and Essential Fatty Acids, 58, 185-191.
20. Marambe, H. K., Shand, P. J., & Wanasundara, J. P. D. (2008). JAOCS, Journal of the American Oil Chemists’ Society, 85, 1155-1164.
21. Kristensen, M., Jensen, M., Aarestrup, J., Petersen, K., Søndergaard, L., Mikkelsen, M. S., et al. (2012). Nutrition & Metabolism, 9, 1-8.
22. Kristensen, M., Knudsen, K. E. B., Jørgensen, H., Oomah, D., B€ugel, S., Toubro, S., et al. (2013). Nutrients, 5, 3287-3298.