Echium oil (EO) is a novel source of omega-3 fatty acids, derived from Echium plantagineum-- a member of the borage family. The oil is a natural source, 12–14 percent, ofstearidonic acid (SDA; 18:4 omega-3),which can be converted by the body to eicosapentaenoic acid(EPA) and docosapentaenoic acid(DPA). It is typically marketed as a vegetarian alternative to fish oils in the omega-3area. EO is also a rich source (33%) of alpha-linolenic acid (ALA) and 12% gamma-linolenic acid (GLA). It is typically marketed as a vegetarian alternative to fish oils in the omega-3area.
SDA is also found in the seed oils of black currant, hemp and borage as well as in newly developed genetically modified soybean oil (Soymega). The fatty acid is of interest, as it is an intermediate in the conversion of ALA to EPA. The critical step in this process is desaturation at the six carbon position ALA. This is believed to be rate limiting and affected by genetic, dietary and environmental factors including aging, stress, diabetes, alcohol, smoking, cholesterol, trans and saturated fatty acid consumption, low omega-3 fatty acid intakes and vitamin and mineral deficiencies.
Research on SDA is relatively new but is expanding at a rapid pace. James et al. (1) reported that dietary SDA is effectively converted to EPA and DPA but not DHA concentrations in erythrocyte and in plasma phospholipids. The relative effectiveness of the tested dietary fatty acids in increasing tissue EPA was 1:0.3:0.07 for EPA:SDA:ALA. Encapsulated SDA, ALA, or EPA (supplied as ethyl esters in capsules) were ingested daily in doses of 0.75g and then 1.5g for periods of three weeks each (n = 15/group) in a double-blind, parallel-group design. The data indicated that 1g dietarySDA is approximately equivalent to 300mg dietary EPA in termsof increasing tissue concentrations of EPA.
The effects of SDA from EO on blood lipids and mononuclear cells have been assessed (2). Healthy young males were randomized to consume one of seven oil blends for a period of 12 weeks (9g oil/day) (n = 8-12 subjects/group). Palm oil, sunflower oil, an EPA-rich oil, borage oil (rich in GLA), and EO were blended in various combinations to generate a placebo oil and oils providing approximately 2g GLA + SDA + EPA per day, but in different combinations. When fed at levels up to 1g/day, SDA did not appear in any of the lipid fractions studied. However, SDA (1g/day), in combination with GLA (0.9g/day), increased the proportion of EPA in some lipid fractions. EPA consumption increased the EPA content of all lipid fractions studied. The authors concluded that SDA may be used as a precursor to increase the EPA content of human lipids.
EO has also been investigated to determine the effects of SDA on serum triacylglycerol (TG) concentrations in hypertriglyceridemichumans (3). Eleven subjects consumed15g of EO daily for four weeks. During the treatment period,serum TG concentrations decreased by 21%, similar to that reported following fish oil supplementation. EPA levels increasedsignificantly in plasma and neutrophils. In addition to SDA, the levels of GLA and ALA in EO may also act independently on serum lipids.
In animal research, SDA has been shown to reduce the production of the pro-inflammatory compound tumor necrosis factor (TNF) by LPS-stimulated whole blood to the same extent as the same amount of dietary ALA or EPA (4). Diets containing synthesized TG mixtures were fed to Balb/c mice for three weeks. In splenocytes, prostaglandin F2 (PGE2) production was suppressed by dietary n-3 PUFA. Whether these effects were due to SDA alone or to its conversion to EPA was not discussed.
A subsequent supplementation experiment usingapoB100 only LDL receptor knockout (B100 only, LDLrKO) mice, an animal model of atherosclerosis that exhibits a mild elevation in plasma TG concentrations has been conducted (5). Basal diets containing 10% calories as palm oil (PO) and 0.2% cholesterol were fed for four weeks, after which mice were randomly assigned to PO, EO or fish oil (FO) for eight weeks. This study showed that SDA in EO is converted to EPA in plasma and liver lipids of the B100 only, LDLrKO mouse.The EO and FO experimental diets decreased plasma TG and VLDL lipid concentration, and hepatic TG content compared to PO. EO fed mice had plasma and liver lipid EPA enrichment that was greater than PO-fed mice but less than FO-fed mice. Down-regulation of several genes involved in hepatic TG biosynthesis was similar for mice fed EO and FO and significantly lower compared to those fed PO.
A follow-up study by the same researchers determined whether EO consumption confers atheroprotection and, if so, to what extent compared to that of FO (6).Male apoB100-only LDLrKO mice were fed one of three diet groups designated as PO, EO, or FO. Consistent with previous research, mice fed EO exhibited enrichment in EPA, but not DHA, relative to those fed PO as well as a rapid, significant, and sustained reduction in plasma TG levels. In this research, aortic lesion surface area was significantly reduced in EO and FO fed mice compared to the PO fed group. Aortic cholesterol concentrations were significantly lower for EO and FO groups in comparison to the PO group. Finally, aortic root intimal area was reduced 17% in EO versus PO fed mice.
As a basis for future studies in humans, the growth, tissue polyunsaturated fatty acid (PUFA) concentrations, and liver lipid profiles in premature neonatal Sprague-Dawley rats fed an EO diet have been compared with those that were dam-fed (DF) or fed a fish oil (FO) diet (7). EO or FO comprised 10% of dietary fat. Compared with DF rats, EO fed rats had similar brain DHA levels, similar brain and liver arachidonic acid (ARA) levels, higher liver and ileal EPA levels and similar ARA:(EPA+DHA) ratios in brain, liver, and serum. EO fed rats had higher ARA levels in brain, liver, ileum, and serum than FO fed rats. The results identify that dietary EO increases tissue EPA and DHA without reducing ARA in brain and liver and without elevating hepatic lipid concentrations of premature neonatal rats. The data suggest that premature neonatal rats can actively synthesize EPA and DHA from SDA derived from dietary EO. The authors concluded that EO could serve as an alternative fat source in preterm infant formula to improve tissue (n-3) long-chain PUFA status in very low birth weight infants, although research is necessary to substantiate this.
The relationship between dosage and duration of consumption of SDA and EPA on EPA enrichment of RBC membranes during a 12-week period has recently been determined (8). An empirical approach was used to derive dosage-specific conversion efficiencies of SDA relative to the range of recommended intake dosages of EPA. An intake of SDA as low as1.3g/d significantly increased RBC% EPA versus a safflower oil control. The researchers reported that at intakes of 0.25 to 0.5g/day EPA, the equivalent intakes of SDA would be 0.6–1.9g/d. At dietary SDA intakes of 1.5–4.0g/d, the efficiency of EPA enrichment in RBC membranes by SDA relative to EPA was 20%, with greater efficiency below and lower efficiency above that range of intakes. These findings suggest that low daily intakes of SDA which are easily achievable through the consumption of EO, has the potential to raise tissue membrane levels of EPA. However, because EO does not result in DHA enrichment equivalent to FO, due to limited delta-6 desaturase mediated conversion of EPA to DHA, EO is not a complete substitute for FO and may not satisfy the body’s essential need for DHA.
Marketing of Echium Oil
In 2008 recognizing the value of EO to consumers and the market, Bioriginal Europe (www.bioriginal.nl) gained a European Union novel foods approval after demonstrating safety to European authorities (9). The company’s EO product, BioMegaSDA was identified as substantially equivalent to the first EO to win novel foods approval -- Croda’s Incromeda V3.
The market for end products with BioMegaSDA is in full development. Several supplement products are available on the market including vegetarian EO capsules and EO plus algal DHA. EO provides an enriched source of SDA that can be converted to EPA and DPA. Research is growing to support similar health benefits as FO, especially with regard to hypertriglyceridemia and cardiovascular disease. EO offers a natural source of SDA which can prove valuable where dietary consumption of EPA is low, e.g. in Westernized countries.
1. James, M.J., Ursin, V.M. and Cleland, L.G. 2003. “Metabolism of Stearidonic Acid in Human Subjects: Comparison with the Metabolism of Other n-3 Fatty Acids.” Amer. J. Clin. Nutr. 77:1140-5.
2. Miles, EA, Bamerjee, T., and Calder, PC. 2004. “The Influence of Different Combinations of Gamma-linolenic, Stearidonic and Eicosapentaenoic Acids on the Fatty Acid Composition of Blood Lipids and Mononuclear Cells in Human Volunteers.” Prostaglandins Leukot. Essent. Fatty Acids.70(6):529-38.
3. Surette, ME, Edens, M., Chilton, F.H. and Tramposch, M. 2004. “Dietary Echium Oil Increases Plasma and Neutrophil Long-Chain (n-3) Fatty Acids and Lowers Serum Triacylglycerols in Hypertriglyceridemic Humans.” J. Nutr. 134:1406-1411.
4. Ishihara, K., Komatsu, W., Saito, H. and Shinohara, K. 2002. “Comparison of the Effects of Dietary Alpha-Linolenic, Stearidonic, and Eicosapentaenoic Acids on Production of Inflammatory Mediators in Mice.” Lipids. 37:481 – 486.
5. Zhang, P., Boudyguina, E., Wilson, M.D., et al. 2008. “Echium Oil Reduces Plasma Lipids and Hepatic Lipogenic Gene Expression in apoB100-only LDL Receptor Knockout Mice.” J Nutr. Biochem. 19:655–63.
6. Forrest, L.M., Boudyguinaa, E., Wilson, M.D., et al. 2011. “Echium Oil Reduces Atherosclerosis in apoB100-only LDLrKO Mice.” Atherosclerosis. doi:10.1016/j.atherosclerosis.2011.10.025.
7. Yang, Q. and O’Shea, T.M. 2009. “Dietary Echium Oil Increases Tissue (n-3) Long-Chain Polyunsaturated Fatty Acids without Elevating Hepatic Lipid Concentrations in Premature Neonatal Rats.” J. Nutr.139: 1353–1359.
8. Krul, E.S., Lemke, R., Mukherjea, M.L. et al. n2011. “Effects of Duration of Treatment and Dosage of Eicosapentaenoic Acid and Stearidonic Acid on Red Blood Cell Eicosapentaenoic Acid Content.” Prostaglandins Leukot. Essent. Fatty Acids. doi:10.1016/j.plefa.2011.10.005.
9. EC (European Commission). 2008. “Commission Decision of 27 June 2008 Authorizing the Placing on the Market of Refined Echium Oil as Novel Food Ingredient Under Regulation (EC) No 258/97 of the European Parliament and of the Council.” OJ L 180, 9.7.2008, pp. 17-19.