Bio Availability of Krill v's Fish Oil
How Krill Oil Works | Bio Availability of Krill V's Fish | Krill Oil and Hyperlipidemia | Capsules
NEPTUNE KRILL OIL (NKO™) BIOAVAILABILITY
Neptune Krill Oil (NKO) has a unique biomolecular profile of omega-3 (EPA/DHA) ™ fatty acids functionalized by their attachment to phospholipids and diverse antioxidants that surpasses 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 their bioavailability and ultimately improving the omega-3: omega-6 ratio.
Scientific data has demonstrated that:
- Fatty acid composition of phospholipids affects cell membrane properties.
- Biochemical synergy between fatty acids, phospholipids and antioxidants is crucial in maintaining omeostasis.
- Phospholipid molecules play a major role in membrane fluidity and nutrient absorption Synergistic choice of fatty acids attached to phospholipids for increased bioavailability and absorption = EPA DHA
- Increased bioavailability and absorption of a nutrient or drug translate to lower effective dose and faster time to effect. The natural combination of the above molecular composition and properties allows NKO™ an almost ideal benefit to risk profile for the management of inflammation and cardiovascular health.
- This is a fact that is proven in our Phase II clinical trial: “Evaluation of the effectiveness of NKO™ on the clinical management of Hyperlipidemia". The results of this clinical trial clearly demonstrate (possibility of error less than 1 in 1000) that 1g of NKO™ as a booster and a maintenance dose of 0.5g is significantly more effective for the regulation of blood lipids and glucose than 3g maximum EPA-DHA fish oil.
- The astaxanthin and the flavonoid (1st flavonoid to be extracted from an animal marine biomass) in NKO™ esterify with a double bond with the EPA and the DHA respectively. This esterification allows the direct metabolism of the antioxidants making them more bioavailable than other antioxidants on the market.
- Because of the abundance of phospholipids in NKO™ it bypasses the stomach and is digested in the small intestine. This explains the fact that even at 12 times the DRI there has been no reported incident of regurgitation. This eliminates the most frequent side effect of fish oils which is the fishy after taste and constant reflux.
RELATED ABSTRACTS
1. Influence of the Physicochemical Form of Polyunsaturated Fatty Acids on Their in vivo Bioavailability.
M. Cansell , N. Moussaoui, A. Denizot and N. Combe , ISTAB/University Bordeaux France, Stéarinerie, Dubois, France, 94th Annual AOC Meting & Expo.
PHO1: Phospholipids for Improving Bioavailability Chair: Michael Schneider,
Consultant, Germany.
For several years now, there has been a growing body of influence on the implication of n-3 fatty acids, and especially polyunsaturated fatty acids (PUFA) on cardiovascular and inflammatory disease prevention. In vivo, PUFA bioavailability depends on several factors such as the type of lipids in which they are esterified, their physical state, i.e., lipid solution or colloidal particle systems and the presence of co-ingested lipids. A study performed in the ISTAB/University Bordeaux and Stéarinerie Dubois in France evaluated the impact of these different parameters on bioavailability in vivo. PUFA were given to rats in the form of liposomes based on a natural marine lipid extract (PUFA esterified in phospholipids organized into bilayer structures), and in the form of fish oil, both dietary lipid form being characterized by a similar fatty acid composition. First, liposomes prepared by direct filtration were tested in vitro for their stability in gastrointestinal-like conditions. Although, acidification favoured liposome size and shape changes, the membrane structures were preserved after an acid stress. No lipid oxidation products were detected during the 14 first hours of incubation at pH 1.5 and 37°C, and phospholipid hydrolysis was less than 15%. These results evidenced that,
indeed, liposomes can be envisaged as oral route PUFA vectors. In vivo PUFA absorption was evaluated by fatty acid analysis of thoracic lymph of duct-cannulated rats, after intragastric feeding of dietary fats. DHA was better absorbed when delivered by liposomes than by fish oil (relative lymphatic absorption equal to 91 % and 65 %, after liposome and fish oil administration, respectively). The best bioavailability of DHA delivered by liposomes was revealed by an increase in DHA proportions in both lymphatic triacylglycerols and phospholipids compared to fish oil diet.
2. Treatment of EFA deficiency with dietary triglycerides or phospholipids in a murine model of extrahepatic cholestasis Anniek Werner, Rick Havinga, Folkert Kuipers, and Henkjan J. Verkade
Department of Pediatrics, Center for Liver, Digestive and Metabolic Diseases Academic Hospital Groningen, 9700 RB Groningen, The Netherlands Am J Physiol Gastrointest Liver Physiol 286: G822-G832, 2004. First published December 11, 2003. Essential fatty acid (EFA) deficiency during cholestasis is mainly due to malabsorption of dietary EFA (23). Theoretically, dietary phospholipids (PL) may have a higher bioavailability than dietary triglycerides (TG) during cholestasis. We developed murine models for EFA deficiency (EFAD) with and without extrahepatic cholestasis and compared the efficacy of oral supplementation of EFA as PL or as TG. EFAD was induced in mice by feeding a high-fat EFAD diet. After 3 wk on this diet, bile duct ligation was performed in a subgroup of mice to establish extrahepatic cholestasis. Cholestatic and noncholestatic EFAD mice continued on the EFAD diet (controls) or were supplemented for 3 wk with EFA-rich TG or EFA-rich PL. Fatty acid composition was determined in plasma, erythrocytes, liver, and brain. After 4 wk of EFAD diet, induction of EFAD was confirmed by a sixfold increased triene-to-tetraene ratio (T/T ratio) in erythrocytes of noncholestatic and cholestatic mice (P < 0.001). EFA-rich TG and EFA-rich PL were equally effective in preventing further increase of the erythrocyte T/T ratio, which was observed in cholestatic and noncholestatic nonsupplemented mice (12- and 16-fold the initial value, respectively). In cholestatic mice, EFA-rich PL was superior to EFA-rich TG in decreasing T/T ratios of liver TG and PL (each P < 0.05) and in increasing brain PL concentrations of the long-chain polyunsaturated fatty acids (LCPUFA) docosahexaenoic acid and arachidonic acid (each P < 0.05).
We conclude that oral EFA supplementation in the form of PL is more effective than in the
form of TG in increasing LCPUFA concentrations in liver and brain of cholestatic EFAD mice.