Evaluation of the effects of Neptune krill oil on the clinical course of hyperlipidemia

Alternative Medicine Review,  Dec, 2004  by Ruxandra Bunea,  Khassan El Farrah,  Luisa Deutsch

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Abstract

OBJECTIVE: To assess the effects of krill oil on blood lipids, specifically total cholesterol, triglycerides, low-density lipoprotein (LDL), and high-density lipoprotein (HDL). METHODS: A multi-center, three-month, prospective, randomized study followed by a three-month, controlled follow-up of patients treated with 1 g and 1.5 g krill oil daily. Patients with hyperlipidemia able to maintain a healthy diet and with blood cholesterol levels between 194 and 348 mg/dL were eligible for enrollment in the trial. A sample size of 120 patients (30 patients/group) was randomly assigned to one of four groups. Group A received krill oil at a body mass index (BMI)-dependent daily dosage of 2-3 g daily. Patients in Group B were given 1-1.5 g krill oil daily, and Group C was given fish oil containing 180 mg eicosapentaenoic acid (EPA) and 120 mg docosahexaenoic acid (DHA) per gram of oil at a dose of 3 g daily. Group D was given a placebo containing microcrystalline cellulose. The krill oil used in this study was Neptune Krill Oil (NKO), provided by Neptune Technologies & Bioresources, Laval, Quebec, Canada. OUTCOME MEASURES: Primary parameters tested (baseline and 90-day visit) were total blood cholesterol, triglycerides, LDL, HDL, and glucose. RESULTS: Krill oil 1-3 g/day (BMI-dependent) was found to be effective for the reduction of glucose, total cholesterol, triglycerides, LDL, and HDL, compared to both fish oil and placebo. CONCLUSIONS: The results of the present study demonstrate within high levels of confidence that krill oil is effective for the management of hyperlipidemia by significantly reducing total cholesterol, LDL, and triglycerides, and increasing HDL levels. At lower and equal doses, krill oil was significantly more effective than fish oil for the reduction of glucose, triglycerides, and LDL levels. (Altern Med Rev 2004;9(4):420-428)

Introduction

The balance of polyunsaturated essential fatty acids (PUFAs) in the body is critical for the maintenance of healthy cell membranes and hormone regulation. During the last few decades the fatty acid content of the U.S. diet has shifted so it now contains much higher levels of omega-6 and less omega-3 fatty acids. When long-chain omega-6 fatty acids predominate in the phospholipids of cell membranes, the production of pro-inflammatory type-2 prostaglandins (PGs) and type-4 leukotrienes (LTs) are encouraged: whereas, the presence of omega-3 fatty acids promotes the production of anti-inflammatory PGs and LTs. (1,2)

Omega-6 fatty acids, mainly arachidonic acid, have been shown to initiate an inflammatory process by triggering a flux of inflammatory PGs and LTs. (34) Omega-3 fatty acids, mainly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), compete with the omega-6 species for the enzyme prostaglandin synthetase. Omega-3 fatty acids trigger secretion of less potent 5-series LTs and anti-inflammatory PGs of the 3 series (P[E.sub.3], P[I.sub.3] and thromboxanes-[A.sub.3]). (4-9) Consequently, supplementation with EPA and DHA promotes the production of less potent PGs and LTs, resulting in a decrease in the formation of inflammatory mediators. (10-13)

The exact mechanism of action by which omega-3 fatty acids favorably modify cardiovascular disease and associated disorders is not yet fully confirmed. Evidence suggests an increased intake of EPA and DHA results in an increase of EPA and DHA in tissue, cellular lipids, and circulatory lipids. (14) In parallel, they result in a simultaneous reduction of omega-6 fatty acids in the body. (14) This fatty acid shift is predominantly marked in cell membrane-bound phospholipids and results in alteration of the physicochemical properties of cell membranes. This favorably modifies cellular functions, including cell signaling, gene expression, biosynthetic processes, and eicosanoid formation. (15)

Human studies have revealed the ability of EPA and DHA to significantly reduce circulating levels of blood triglyceride and very low-density lipoprotein (VLDL), which have been associated with increased risk of cardiovascular disease. (16,17)

Krill oil is extracted from Antarctic krill, Euphausia superba, a zooplankton crustacean rich in phospholipids carrying long-chain omega-3 PUFAs, mainly EPA and DHA. Krill oil also contains various potent antioxidants, including vitamins A and E, astaxanthin, and a novel flavonoid similar to 6,8-di-c-glucosylluteolin, but with two or more glucose molecules and one aglycone.

Krill oil has a unique biomolecular profile of phospholipids naturally rich in omega-3 fatty acids and diverse antioxidants significantly different from the usual profile of fish oils. The association between phospholipids and long-chain omega-3 fatty acids highly facilitates the passage of fatty acid molecules through the intestinal wall, increasing bioavailability and ultimately improving the omega-3:omega-6 fatty acid ratio. (18,19)

Materials and Methods

A 12-week, double-blind, randomized trial was conducted comparing krill oil to high EPA and DHA (3:2 ratio) fish oil and placebo. Eligible patients were 18-85 years and had at least a six-month diagnosis of mildly high to very high blood cholesterol (193.9-347.9 mg/dL) and triglyceride levels (203.8-354.4 mg/dL). Patients with familial hypercholesterolemia, severely high cholesterol (>349 mg/dL), pregnancy, known or suspected allergy to fish or seafood, known alcohol or drug abuse within the previous year, known coagulopathy or receiving anticoagulant therapy, or co-morbidity that would interfere with study results were excluded from the study.