Omega-7 Protects Against Metabolic Syndrome

 

Most people are aware of the wide-ranging benefits of omega-3 fatty acids, but you likely aren’t aware of a category of omega-7 fats that provide some unique health effects.

Scientists have recently uncovered a specific kind of omega-7 called palmitoleic acid. This newly discovered fat molecule is so important that Harvard Medical School has applied for a patent on it.¹

What’s so special about this particular omega-7?

It powerfully addresses many of the underlying factors involved in metabolic syndrome.^2-7 This feat would require multiple prescription drugs to achieve⁸—with potentially dangerous side effects. Omega-7 palmitoleic acid can safely do all this at a fraction of the cost.

Omega-7 can reduce risk of type II diabetes, prevent the buildup of atherosclerotic plaque, increase beneficial HDL and lower an inflammation marker called C-reactive protein, which is associated with an increased risk for heart attack and stroke.^3,5,7,9

In these ways, omega-7 is able to powerfully—and affordably reduce risk of the negative consequences of metabolic syndrome—including heart disease, diabetes, cancer, and other life-threatening disorders.

What Is Palmitoleic Acid?

Palmitoleic acid is a member of the class called omega-7 fatty acids. Omega-7s include several different fatty acids. For the purposes of this article, when we refer to omega-7, we’re referring to palmitoleic acid.

Unlike the better known polyunsaturated omega-3s, omega-7s are monounsaturated fats.¹⁰ And while omega-3 fatty acids are beneficial largely because they become incorporated into anti-inflammatory molecules,¹¹ omega-7s have an entirely different mechanism of action. Omega-7 fats function as signaling molecules that facilitate communication between fat and muscle tissue in your body.¹²

This special signaling function qualifies omega-7 to be identified as a unique lipokine—a hormone-like molecule that links distant body tissues to assure optimal energy utilization and storage.¹²

That’s what allows omega-7 to have broad-reaching effects on various factors of metabolic syndrome.^2-7,13

Ingestion of just a small amount of omega-7 has a profound effect on the body’s response to energy intake, fat storage, and utilization, all of which are imbalanced in metabolic syndrome. Omega-7 suppresses the production of new fat molecules, especially those fats that damage tissue and raise cardiovascular risk.^2,14

In fact, omega-7’s beneficial effects resemble those of many drugs (such as Lipitor^®, Actos^®, Lopid^®, and others) commonly used by people with high cholesterol and/or high blood sugar, major elements of metabolic syndrome that increase the risk of cardiovascular disease.

Omega-7 Fights The Factors Of Metabolic Syndrome

 

As medically defined, metabolic syndrome, a major contributor to cardiovascular disease risk and type II diabetes, consists of:^15-17

1. Elevated glucose and insulin resistance.
2. Lipid disturbances (high triglycerides and low HDL cholesterol).
3. High blood pressure.
4. Central obesity (“apple shape”).
5. Chronic inflammation.

Even though chronic inflammation is not technically a criterion for metabolic syndrome, it is widely recognized as a fifth major pathological contributor to the condition.^15,17,18

If you have metabolic syndrome, it means you are already well along the road to heart disease, diabetes, cancer, and other life-threatening disorders.¹⁶ Fortunately, omega-7 works in five distinct and complementary ways to reduce most of metabolic syndrome’s harmful effects on your health:

1. It reduces insulin resistance and lowers blood glucose.^3,4
2. It suppresses fat production and accumulation.^2,3
3. It normalizes abnormal lipid profiles (including raising beneficial HDL-cholesterol).^3,5-7
4. It fights obesity.^3,13
5. It powerfully suppresses the inflammation that drives metabolic syndrome.^3,7

We will break down each of the factors one at a time in order to see how omega-7 addresses the various contributing factors involved in metabolic syndrome, ultimately reducing risk of cardiovascular disease, diabetes, cancer, and more.

What You Need to Know

Guard Against Metabolic Disturbances With Omega-7

• A new healthy fatty acid, omega-7 palmitoleic acid, has joined the ranks of omega-3 fats in protecting your body from the dreaded metabolic syndrome.
• Adding omega-7 to your supplement regimen can help your body mitigate many of the components of metabolic syndrome, including high LDL and low HDL cholesterol, high glucose and insulin resistance, obesity, and even the inflammation that drives the syndrome.
• Big Pharma has at least four categories of drugs to treat metabolic syndrome, but these carry various side effect profiles and can interact negatively with one another.
• Omega-7 may help you reduce the burden of metabolic syndrome in your own body.
• Add omega-7 palmitoleic acid to your omega-3 regimen today to optimize your cardiovascular and metabolic health.

Omega-7 Fights Inflammation

There’s a close connection between fat tissue and the chronic, low-grade inflammation that’s associated with metabolic syndrome.^17-19 The connection may be related to an enzyme known as SCD1 (stearoyl-CoA desaturase 1).

When scientists remove SCD1 activity in lab animals, their levels of fat tissue inflammation fall sharply, and their ability to respond to insulin (insulin sensitivity) rises.²⁰ In the lab, adding omega-7 to cultures of fat cells triggers these same benefits by suppressing SCD1 activity.²

Animal studies show significantly reduced levels of fat-related inflammatory cytokines (signaling molecules) following administration of omega-7.³ And the livers of supplemented animals show significant reductions in the number of activated inflammatory cells, an effect that may help prevent fatty liver disease.²¹ Many of these beneficial anti-inflammatory effects may arise from the ability of omega-7 to deactivate the master inflammatory regulation complex called NF-kappaB.²¹

There’s now impressive human data on how omega-7 can lower inflammation and reduce the resulting cardiovascular risk. In a pilot trial of adults with high levels of C-reactive protein (blood marker of inflammation), supplementation with 210 mg a day of omega-7 resulted in a robust 73% decrease of C-reactive protein.⁶

Those results were extended in a larger, randomized clinical trial, in which all patients had abnormally high CRP levels (greater than 3 mg/dL). In this study, 30 days of supplementation with 210 mg/day of palmitoleic acid resulted in a significant drop in CRP of 1.9 mg/dL — that’s a 43% reduction in a dangerous cardiovascular risk marker. Moreover, by the end of the supplementation period, the average CRP level was reduced from greater than 4 mg/dL to 2.1 mg/dL.⁷ The health ramifications of this marked reduction in C-reactive protein are profound, especially in abdominally-obese individuals who often exhibit dangerously elevated levels of this inflammatory indicator (CRP).

Omega-7 Lowers Glucose And Insulin Resistance

Omega-7 has multiple beneficial effects on blood sugar and insulin. Researchers discovered that when mice with type II diabetes were supplemented with omega-7, they had lower blood glucose and triglyceride levels. ³ At the same time, their insulin resistance and liver fat deposits were significantly reduced. Liver fat deposition is a key factor in metabolic syndrome, and is a leading cause of non-alcoholic fatty liver disease, or NAFLD.³ These animals also experienced decreases in diabetes-related weight gain, and reduced levels of inflammatory cytokines.

Omega-7 produces these encouraging results because it attacks multiple underlying mechanisms responsible for type II diabetes/insulin resistance.

In metabolic syndrome as well as in type II diabetes, the body’s cells become resistant to the sugar-lowering effects of insulin. This results in rising sugar levels, and also rising levels of insulin, both of which are toxic in large quantities. Omega-7 counteracts this by doubling glucose uptake by muscle cells, increasing their ability to burn sugar for energy and store it in quick-release, non-toxic glycogen.²²

What happens next is that when your body’s cells become resistant to the sugar-lowering effects of insulin, blood sugar will eventually rise. Pancreatic cells that produce insulin are among the casualties of high glucose, eventually resulting in still higher sugar levels and worse tissue damage.²³ Omega-7 protects the insulin-producing cells of the pancreas from glucose-induced toxicity; in fact, omega-7 enhances proliferation of pancreatic beta cells, helping your body optimize blood sugar control with its own natural insulin.²⁴

Omega-7 levels strongly predict insulin sensitivity: One’s odds of having beneficially high insulin sensitivity rise dramatically as their blood omega-7 levels rise.⁴

All Omega-7 Sources Are Not The Same

While you can get omega-7 palmitoleic acid from some natural sources, such as macadamia nuts and sea buckthorn, it’s important that you be aware that these foods also contain very high levels of palmitic acid. Palmitic acid is a thick, gooey palm oil.

Palmitic acid consumption raises the risk of heart attack, stroke, and other cardiovascular catastrophes by increasing arterial stiffness, triggering abnormal platelet clumping, and raising dangerous LDL cholesterol levels.^55-57

Sea buckthorn and macadamia oils typically contain around 11 to 27% omega-7 (which is good) but they also contain around 9 to 40% palmitic acid, which can largely negate the benefits of the omega-7.^58,59

That’s why it’s vital that you use an omega-7 product that is purified to reduce the palmitic acid concentration to less than 1%, and also ideally concentrated to raise the omega-7 content to near 50%.

Palmitoleic Acid Improves Arterial Health

Omega-7’s ability to raise HDL and lower LDL—while also supporting endothelial function—make it extremely beneficial for cardiovascular health.

Studies show that omega-7 improves lipid balance by favorably regulating fat production within fat cells, while regulating fat burning.² That means less fat deposition—and lower levels of fat and triglycerides in blood and liver tissue.^3,25

In a lab study done at the Cleveland Clinic, omega-7 supplementation increased beneficial HDL after just 8 to 12 weeks (something statin drugs are not very good at doing).^5,26,27 In the same study, the reduction in the size of atherosclerotic plaque in the aorta was 47% lower in the group receiving omega-7 supplementation.⁵

Omega-7 levels have also been shown to be powerful predictors of the all-important endothelial function, the control of blood flow and pressure by the inner lining, or endothelium, of blood vessels.²⁸

 

These beneficial effects on cholesterol were demonstrated by a study using macadamia nuts and sea buckthorn, two substances that are known for their high omega-7 content. Studies show that after just three weeks of eating macadamia nuts every day, healthy young women had reductions in total and LDL cholesterol, body weight, and body mass index (BMI).²⁹ And in men with high cholesterol, 1 to 3 ounces per day of these fat-containing nuts produced reductions in atherosclerosis risk factors such as markers of inflammation and oxidative stress.³⁰

These studies may have shown greater effects had the subjects used a purified omega-7 palmitoleic acid supplement instead of the high-fat macadamia nuts, which are also rich in dangerous palmitic acid.

In a study of patients with stubbornly high lipid levels, a purified omega-7 supplement (840 mg/day) produced modest lipid reductions. LDL fell by 7.6% (from 118 to 109 mg/dL) while non-HDL cholesterol* was reduced by 8.2% (from 147 to 135 mg/dL).⁶ Patients with the highest levels of baseline triglycerides saw their total cholesterol and triglyceride levels drop by as much as 30%.⁶

* (Non-HDL cholesterol is gaining increasing importance as a risk marker for cardiovascular outcomes.⁶ It is calculated as total cholesterol minus HDL cholesterol.)

What makes that study remarkable is that most participants were already taking statin or fibrate drugs, yet still had high lipid levels.²⁵ This showed that adding omega-7 to these drugs produced additional benefits, lowering cholesterol and triglycerides where prescription drugs couldn’t.

In a subsequent controlled clinical trial, patients taking purified omega-7 palmitoleic acid at a lower dose (210 mg/day) had improvements in lipid levels after 30 days of supplementation: triglycerides dropped by 36.9 mg/dL (17%), LDL by 13.5 mg/dL (11%), and beneficial HDL rose by 4.5 mg/dL (10%).⁷

Omega-7 Helps Manage Body Weight

The reason central or abdominal obesity (“apple shape”) is a factor in metabolic syndrome is because it has such strong associations with cardiovascular disease risk.³¹ This is due, in large part, to the increased inflammation produced by fat tissue.^17-19

Omega-7s help manage this factor of metabolic syndrome because they signal your body to stop storing fat.^2,3

Animals fed diets rich in omega-7 show significant increases in stomach and intestinal hormones that promote the feeling of fullness (satiety).¹³ At the same time, such diets produce decreases in hunger-promoting hormones.³² The combined effect is a significant reduction in food intake.

Several statin drugs, while lowering cholesterol and triglycerides, also produce increases in body and liver fat deposition.³³ Omega-7s do just the opposite. Omega-7 reduces the production of fat in the liver.³ Increases in liver fat can result in non-alcoholic fatty liver disease (NAFLD), which is considered a major manifestation of the metabolic syndrome—and which can eventually lead to liver failure and even cancer.³⁴

Summary

Research has shown that omega-7 has beneficial effects on a majority of the pathological components of metabolic syndrome.

It improves insulin sensitivity, lowers LDL-cholesterol-triglycerides, and raises beneficial HDL.^3,5,22,24,29 It helps manage body weight by promoting fullness-inducing hormones and dissipating hunger-producing hormones.^13,32 Perhaps most important of all, omega-7 acts in a unique fashion to stop the inflammation that forms the link between the metabolic syndrome and its life-shortening consequences.^3,21

By beneficially influencing these deadly pathological factors, omega-7 can dramatically improve cardiovascular and metabolic health.

If you have any questions on the scientific content of this article, please call a Life Extension^® Health Advisor at 1-866-864-3027.

References

1. Cao H, Hotamisligil G, Inventors; President and Fellows of Harvard College, Cambridge, MA, assignee. Fatty acid C16: 1N7-Palmitoleate a lipokine and biomarker for metabolic status. September 1, 2011.
2. Burns TA, Duckett SK, Pratt SL, Jenkins TC. Supplemental palmitoleic (C16:1 cis-9) acid reduces lipogenesis and desaturation in bovine adipocyte cultures. J Anim Sci. 2012 Oct;90(10):3433-41.
3. Yang ZH, Miyahara H, Hatanaka A. Chronic administration of palmitoleic acid reduces insulin resistance and hepatic lipid accumulation in KK-Ay Mice with genetic type 2 diabetes. Lipids Health Dis. 2011;10:120.
4. Stefan N, Kantartzis K, Celebi N, et al. Circulating palmitoleate strongly and independently predicts insulin sensitivity in humans. Diabetes Care. 2010 Feb;33(2):405-7.
5. Experimental Animal Laboratory. Final report for study onCCO Technologies Oil (CCO-Oil) on the development of atherosclerosis: Department of Cardiovascular Medicine, Cleveland Clinic; 2008.
6. Green JA. Effect of two levels of Provinal™ (purified Palmitoleic Acid; C16:1n7; Omega 7) on serum lipid and C-reactive protein(CRP) profiles in humans. Tersus Pharmaceuticals, LLC: 2012.
7. Martinez L. Provinal (R) in the reduction of CRP: A double blinded, randomized, placebo controlled study. Provinal purified omega 7. Vol: Tersus Pharmaceuticals; 2013.
8. Marcus AO. Safety of drugs commonly used to treat hypertension, dyslipidemia, and type 2 diabetes (the metabolic syndrome): part 1. Diabetes Technol Ther. 2000 Spring;2(1):101-10.
9. Available at: http://circ.ahajournals.org/content/108/12/e81.full. Accessed January 24, 2014.
10. Nestel P, Clifton P, Noakes M. Effects of increasing dietary palmitoleic acid compared with palmitic and oleic acids on plasma lipids of hypercholesterolemic men. J Lipid Res. 1994 Apr;35(4):656-62.
11. Calder PC. Dietary modification of inflammation with lipids. Proc Nutr Soc. 2002 Aug;61(3):345-58.
12. Cao H, Gerhold K, Mayers JR, Wiest MM, Watkins SM, Hotamisligil GS. Identification of a lipokine, a lipid hormone linking adipose tissue to systemic metabolism. Cell. 2008 Sep 19;134(6):933-44.
13. Yang ZH, Takeo J, Katayama M. Oral administration of omega-7 palmitoleic acid induces satiety and the release of appetite-related hormones in male rats. Appetite. 2013 Jun;65:1-7.
14. Burns TA, Kadegowda AK, Duckett SK, Pratt SL, Jenkins TC. Palmitoleic (16:1 cis-9) and cis-vaccenic (18:1 cis-11) acid alter lipogenesis in bovine adipocyte cultures. Lipids. 2012 Dec;47(12):1143-53.
15. Available at: http://www.ersnet.org/learning_resources_player/paper/rs/51.pdf. Accessed January 24, 2014.
16. Available at: http://www.nhlbi.nih.gov/health/health-topics/topics/ms. Accessed January 8, 2014.
17. Available at: http://circ.ahajournals.org/content/109/3/433.full. Accessed January 8, 2014.
18. Festa A, D’Agostino R Jr, Howard G, Mykkänen L, Tracy RP, Haffner SM. Chronic subclinical inflammation as part of the insulin resistance syndrome: the Insulin Resistance Atherosclerosis Study (IRAS). Circulation. 2000 Jul 4;102(1):42-7.
19. Shah A, Mehta N, Reilly MP. Adipose inflammation, insulin resistance, and cardiovascular disease. JPEN J Parenter Enteral Nutr. 2008 Nov-Dec;32(6):638-44.
20. Liu X, Miyazaki M, Flowers MT, et al. Loss of Stearoyl-CoA desaturase-1 attenuates adipocyte inflammation: effects of adipocyte-derived oleate. Arterioscler Thromb Vasc Biol. 2010 Jan;30(1):31-8.
21. Guo X, Li H, Xu H, et al. Palmitoleate induces hepatic steatosis but suppresses liver inflammatory response in mice. PLoS One. 2012;7(6):e39286.
22. Dimopoulos N, Watson M, Sakamoto K, Hundal HS. Differential effects of palmitate and palmitoleate on insulin action and glucose utilization in rat L6 skeletal muscle cells. Biochem J. 2006 Nov 1;399(3):473-81.
23. Prentki M, Nolan CJ. Islet beta cell failure in type 2 diabetes. J Clin Invest. 2006 Jul;116(7):1802-12.
24. Maedler K, Spinas GA, Dyntar D, Moritz W, Kaiser N, Donath MY. Distinct effects of saturated and monounsaturated fatty acids on beta-cell turnover and function. Diabetes. 2001 Jan;50(1):69-76.
25. Shiba S, Tsunoda N, Wakutsu M, et al. Regulation of lipid metabolism by palmitoleate and eicosapentaenoic acid (EPA) in mice fed a high-fat diet. Biosci Biotechnol Biochem. 2011;75(12):2401-3.
26. Chang YH, Lin KC, Chang DM, Hsieh CH, Lee YJ. Paradoxical negative HDL cholesterol response to Atorvastatin and Simvastatin treatment in Chinese type 2 diabetic patients. Rev Diabet Stud. 2013 Summer;10(2-3):213-22.
27. Asztalos BF, Horvath KV, McNamara JR, Roheim PS, Rubinstein JJ, Schaefer EJ. Comparing the effects of five different statins on the HDL subpopulation profiles of coronary heart disease patients. Atherosclerosis. 2002 Oct;164(2):361-9.
28. Sarabi M, Vessby B, Millgard J, Lind L. Endothelium-dependent vasodilation is related to the fatty acid composition of serum lipids in healthy subjects. Atherosclerosis. 2001 Jun;156(2):349-55.
29. Hiraoka-Yamamoto J, Ikeda K, Negishi H, et al. Serum lipid effects of a monounsaturated (palmitoleic) fatty acid-rich diet based on macadamia nuts in healthy, young Japanese women. Clin Exp Pharmacol Physiol. 2004 Dec;31 Suppl 2:S37-8.
30. Garg ML, Blake RJ, Wills RB, Clayton EH. Macadamia nut consumption modulates favourably risk factors for coronary artery disease in hypercholesterolemic subjects. Lipids. 2007 Jun;42(6):583-7.
31. Elbassuoni E. Better association of waist circumference with insulin resistance and some cardiovascular risk factors than body mass index. Endocr Regul. 2013 Jan;47(1):3-14.
32. Lu X, Zhao X, Feng J, et al. Postprandial inhibition of gastric ghrelin secretion by long-chain fatty acid through GPR120 in isolated gastric ghrelin cells and mice. Am J Physiol Gastrointest Liver Physiol. 2012 Aug 1;303(3):G367-76.
33. Aguirre L, Hijona E, Macarulla MT, et al. Several statins increase body and liver fat accumulation in a model of metabolic syndrome. J Physiol Pharmacol. 2013 Jun;64(3):281-8.
34. Pappachan JM, Antonio FA, Edavalath M, Mukherjee A. Non-alcoholic fatty liver disease: a diabetologist’s perspective. Endocrine. 2013 Nov 28.
35. Cignarelli A, Giorgino F, Vettor R. Pharmacologic agents for type 2 diabetes therapy and regulation of adipogenesis. Arch Physiol Biochem. 2013 Oct;119(4):139-50.
36. Dzien A, Winner H, Theurl E, Dzien-Bischinger C, Lechleitner M. Fat-free mass and fasting glucose values in patients with and without statin therapy assigned to age groups between <60 and >75 years. Obes Facts. 2013;6(1):9-16.
37. Fonseca VA. Management of diabetes mellitus and insulin resistance in patients with cardiovascular disease. Am J Cardiol. 2003 Aug 18;92(4a):50j-60j.
38. Greque GV, Serrano CV, Jr., Strunz CM, et al. Preprocedural statin therapy, inflammation and myocardial injury in low-risk stable coronary artery disease patients submitted to coronary stent implantation. Catheter Cardiovasc Interv. 2013 Apr 16.
39. Larsen PJ, Jensen PB, Sorensen RV, et al. Differential influences of peroxisome proliferator-activated receptors gamma and -alpha on food intake and energy homeostasis. Diabetes. 2003 Sep;52(9):2249-59.
40. Oh TJ, Shin JY, Kang GH, Park KS, Cho YM. Effect of the combination of metformin and fenofibrate on glucose homeostasis in diabetic Goto-Kakizaki rats. Exp Mol Med. 2013;45:e30.
41. Saremi A, Schwenke DC, Buchanan TA, et al. Pioglitazone slows progression of atherosclerosis in prediabetes independent of changes in cardiovascular risk factors. Arterioscler Thromb Vasc Biol. 2013 Feb;33(2):393-9.
42. Sattar N, Preiss D, Murray HM, et al. Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials. Lancet. 2010 Feb 27;375(9716):735-42.
43. Tenenbaum A, Fisman EZ. Fibrates are an essential part of modern anti-dyslipidemic arsenal: spotlight on atherogenic dyslipidemia and residual risk reduction. Cardiovasc Diabetol. 2012;11:125.
44. Wang W, Lin Q, Lin R, et al. PPARalpha agonist fenofibrate attenuates TNF-alpha-induced CD40 expression in 3T3-L1 adipocytes via the SIRT1-dependent signaling pathway. Exp Cell Res. 2013 Jun 10;319(10):1523-33.
45. Yoon JS, Lee HW. Diabetogenic effect of statins: A double-edged sword? Diabetes Metab J. 2013 Dec;37(6):415-22.
46. Brindisi MC, Guiu B, Duvillard L, et al. Liver fat content is associated with an increase in cholesterol synthesis independent of statin therapy use in patients with type 2 diabetes. Atherosclerosis. 2012 Oct;224(2):465-8.
47. Available at: http://www.medscape.com/viewarticle/555407_5. Accessed January 13, 2014.
48. Monami M, Vitale V, Ambrosio ML, et al. Effects on lipid profile of dipeptidyl peptidase 4 inhibitors, pioglitazone, acarbose, and sulfonylureas: meta-analysis of placebo-controlled trials. Adv Ther. 2012 Sep;29(9):736-46.
49. Celinski K, Dworzanski T, Fornal R, et al. Comparison of anti-inflammatory properties of peroxisome proliferator-activated receptor gamma agonists rosiglitazone and troglitazone in prophylactic treatment of experimental colitis. J Physiol Pharmacol. 2013 Oct;64(5):587-95.
50. Petrazzi L, Grassi D, Polidoro L, et al. Cardiovascular risk and cardiometabolic protection: role of glitazones. J Nephrol. 2008 Nov-Dec;21(6):826-35.
51. Available at: http://www.nytimes.com/health/guides/disease/type-2-diabetes/medications.html. Accessed January 13, 2014.
52. Cefalu JT, Bell-Farrow A, Wang ZQ, McBride D, Dalgleish D, Terry JG. Effect of glipizide GITS on insulin sensitivity, glycemic indices, and abdominal fat composition in NIDDM. Drug Dev Res.1998 May;44(1):1-7.
53. Available at: http://care.diabetesjournals.org/content/7/6/575.full.pdf. Accessed January 13, 2014.
54. Available at: http://care.diabetesjournals.org/content/32/suppl_2/s337.full. Accessed January 13, 2014.
55. Connor WE. Harbingers of coronary heart disease: dietary saturated fatty acids and cholesterol. Is chocolate benign because of its stearic acid content? Am J Clin Nutr. 1999 Dec;70(6):951-2.
56. Mizurini DM, Maia IC, Sardinha FL, Monteiro RQ, Ortiz-Costa S, do Carmo MG. Venous thrombosis risk: effects of palm oil and hydrogenated fat diet in rats. Nutrition. 2011 Feb;27(2):233-8.
57. Anderson SG, Sanders TA, Cruickshank JK. Plasma fatty acid composition as a predictor of arterial stiffness and mortality. Hypertension. 2009 May;53(5):839-45
58. Yang B, Kallio HP. Fatty acid composition of lipids in sea buckthorn (Hippophaë rhamnoides L.) berries of different origins. J Agric Food Chem. 2001 Apr;49(4):1939-47.
59. Corporate data on file. Fatty acid profile: Tersus Pharmaceutical; 2013.