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1.
Lipids Health Dis ; 14: 142, 2015 Nov 04.
Article En | MEDLINE | ID: mdl-26537218

BACKGROUND: Bioavailability of krill oil has been suggested to be higher than fish oil as much of the EPA and DHA in krill oil are bound to phospholipids (PL). Hence, PL content in krill oil might play an important role in incorporation of n-3 PUFA into the RBC, conferring properties that render it effective in reducing cardiovascular disease (CVD) risk. The objective of the present trial was to test the effect of different amounts of PL in krill oil on the bioavailability of EPA and DHA, assessed as the rate of increase of n-3 PUFA in plasma and RBC, in healthy volunteers. METHODS AND DESIGN: In a semi randomized crossover single blind design study, 20 healthy participants consumed various oils consisting of 1.5 g/day of low PL krill oil (LPL), 3 g/day of high PL krill oil (HPL) or 3 g/day of a placebo, corn oil, for 4 weeks each separated by 8 week washout periods. Both LPL and HPL delivered 600 mg of total n-3 PUFA/day along with 600 and 1200 mg/day of PL, respectively. RESULTS: Changes in plasma EPA, DPA, DHA, total n-3 PUFA, n-6:n-3 ratio and EPA + DHA concentrations between LPL and HPL krill oil supplementations were observed to be similar. Intake of both forms of krill oils increased the RBC level of EPA (p < 0.001) along with reduced n-6 PUFA (LPL: p < 0.001: HPL: p = 0.007) compared to control. HPL consumption increased (p < 0.001) RBC concentrations of EPA, DPA, total and n-3 PUFA compared with LPL. Furthermore, although LPL did not alter RBC n-6:n-3 ratio or the sum of EPA and DHA compared to control, HPL intake decreased (p < 0.001) n-6:n-3 ratio relative to control with elevated (p < 0.001) sum of EPA and DHA compared to control as well as to LPL krill oil consumption. HPL krill oil intake elevated (p < 0.005) plasma total and LDL cholesterol concentrations compared to control, while LPL krill oil did not alter total and LDL cholesterol, relative to control. CONCLUSIONS: The results indicate that krill oil with higher PL levels could lead to enhanced bioavailability of n-3 PUFA compared to krill oil with lower PL levels. TRIAL REGISTRATION: Clinicaltrials.gov# NCT01323036.


Docosahexaenoic Acids/administration & dosage , Eicosapentaenoic Acid/administration & dosage , Erythrocytes/metabolism , Phospholipids/metabolism , Adolescent , Adult , Animals , Cross-Over Studies , Dietary Supplements , Docosahexaenoic Acids/pharmacokinetics , Eicosapentaenoic Acid/pharmacokinetics , Euphausiacea/chemistry , Female , Humans , Male , Middle Aged , Young Adult
2.
Nutr Metab Cardiovasc Dis ; 25(12): 1132-9, 2015 Dec.
Article En | MEDLINE | ID: mdl-26552742

BACKGROUND AND AIM: Compared to a DASH-type diet, an intensively applied dietary portfolio reduced diastolic blood pressure at 24 weeks as a secondary outcome in a previous study. Due to the importance of strategies to reduce blood pressure, we performed an exploratory analysis pooling data from intensively and routinely applied portfolio treatments from the same study to assess the effect over time on systolic, diastolic and mean arterial pressure (MAP), and the relation to sodium (Na(+)), potassium (K(+)), and portfolio components. METHODS AND RESULTS: 241 participants with hyperlipidemia, from four academic centers across Canada were randomized and completed either a DASH-type diet (control n = 82) or a dietary portfolio that included, soy protein, viscous fibers and nuts (n = 159) for 24 weeks. Fasting measures and 7-day food records were obtained at weeks 0, 12 and 24, with 24-h urines at weeks 0 and 24. The dietary portfolio reduced systolic, diastolic and mean arterial blood pressure compared to the control by 2.1 mm Hg (95% CI, 4.2 to -0.1 mm Hg) (p = 0.056), 1.8 mm Hg (CI, 3.2 to 0.4 mm Hg) (p = 0.013) and 1.9 mm Hg (CI, 3.4 to 0.4 mm Hg) (p = 0.015), respectively. Blood pressure reductions were small at 12 weeks and only reached significance at 24 weeks. Nuts, soy and viscous fiber all related negatively to change in mean arterial pressure (ρ = -0.15 to -0.17, p ≤ 0.016) as did urinary potassium (ρ = -0.25, p = 0.001), while the Na(+)/K(+) ratio was positively associated (ρ = 0.20, p = 0.010). CONCLUSIONS: Consumption of a cholesterol-lowering dietary portfolio also decreased blood pressure by comparison with a healthy DASH-type diet. CLINICAL TRIAL REG. NO.: NCT00438425, clinicaltrials.gov.


Cardiovascular Diseases/diet therapy , Diet Records , Diet, Fat-Restricted/methods , Diet, Sodium-Restricted/methods , Hyperlipidemias/diet therapy , Hypertension/diet therapy , Adult , Aged , Blood Pressure Determination/methods , Canada , Cardiovascular Diseases/prevention & control , Diet, Mediterranean , Energy Intake , Female , Follow-Up Studies , Humans , Hyperlipidemias/prevention & control , Hypertension/prevention & control , Male , Middle Aged , Risk Assessment , Treatment Outcome
3.
Eur J Clin Nutr ; 64(7): 660-8, 2010 Jul.
Article En | MEDLINE | ID: mdl-20485301

Resveratrol (RS), a polyphenol compound found in grapes and grape products, including wine, peanuts and berries, exists in cis- and trans-isomeric forms. RS is believed to decrease circulating low-density lipoprotein cholesterol levels and reduce cardiovascular disease (CVD) risk. However, it is possible that RS has other mechanisms to reduce the risk of CVD without altering lipid levels. The objective of this review is to critically examine results from recent research concerning potential effects of RS on CVD. RS exerts several health benefits including anti-atherogenic, anti-inflammatory and anti-cancer effects. RS may also prevent lipid oxidation, platelet aggregation, arterial vasodilation and modulates the levels of lipids and lipoproteins. As a potent, anti-oxidant RS reduces oxidative stress and regenerates alpha-tocopherol, which further strengthens the anti-oxidant defense mechanism. RS has been considered safe as no significant toxic effects have been identified, even when consumed at higher concentrations. This evidence identified RS as an effective anti-atherogenic agent, which could be used in the prevention and treatment of CVD.


Antioxidants/pharmacology , Atherosclerosis/prevention & control , Cardiovascular Diseases/prevention & control , Phytotherapy , Plant Extracts/pharmacology , Stilbenes/pharmacology , Animals , Antioxidants/therapeutic use , Humans , Lipids/blood , Plant Extracts/therapeutic use , Resveratrol , Stilbenes/therapeutic use , Vitis/chemistry
4.
Eur J Clin Nutr ; 63(7): 813-20, 2009 Jul.
Article En | MEDLINE | ID: mdl-19491917

Phytosterol and stanol (or phytosterols) consumption reduces intestinal cholesterol absorption, leading to decreased blood LDL-cholesterol levels and lowered cardiovascular disease risk. However, other biological roles for plant sterols and stanols have also been proposed. The objective of this review is to critically examine results from recent research regarding the potential effects and mechanisms of action of phytosterols on forms of cancer. Considerable emerging evidence supports the inhibitory actions of phytosterols on lung, stomach, as well as ovarian and breast cancer. Phytosterols seem to act through multiple mechanisms of action, including inhibition of carcinogen production, cancer-cell growth, angiogenesis, invasion and metastasis, and through the promotion of apoptosis of cancerous cells. Phytosterol consumption may also increase the activity of antioxidant enzymes and thereby reduce oxidative stress. In addition to altering cell-membrane structure and function, phytosterols probably promote apoptosis by lowering blood cholesterol levels. Moreover, consumption of phytosterols by healthy humans at the recommended level of 2 g per day does not cause any major health risks. In summary, mounting evidence supports a role for phytosterols in protecting against cancer development. Hence, phytosterols could be incorporated in diet not only to lower the cardiovascular disease risk, but also to potentially prevent cancer development.


Anticarcinogenic Agents , Neoplasms/prevention & control , Phytosterols , Animals , Anticarcinogenic Agents/administration & dosage , Anticarcinogenic Agents/metabolism , Anticarcinogenic Agents/pharmacology , Apoptosis/drug effects , Diet , Humans , Neoplasms/pathology , Phytosterols/administration & dosage , Phytosterols/metabolism , Phytosterols/pharmacology
5.
Cell Biochem Funct ; 24(4): 333-40, 2006.
Article En | MEDLINE | ID: mdl-15912568

Neutrophils play an important role in the pathogenesis of rheumatoid arthritis (RA) and various inflammatory conditions, by accumulation and liberation of active proteolytic enzymes. The effect of milk extract of Semecarpus anacardium Linn. nuts (SA) at a dosage of 150 mg kg(-1) body weight day(-1) for 14 days on adjuvant arthritis was studied to gain some insight into this intriguing disease in relation to neutrophil functions. The decreased phagocytic function of neutrophils (phagocytic index and avidity index) found in adjuvant arthritis was significantly increased by the administration of the drug SA. Increased levels of reactive oxygen species (superoxide radical, hydroxyl radical, H2O2 and myeloperoxidase), lysosomal enzymes (acid phosphatase and cathepsin D) and increased accumulation of neutrophils in the joints observed in adjuvant arthritic animals were reverted back to near normal levels by treatment with SA. The results of this study indicate that SA can be considered to be a good therapeutic agent for inflammation and arthritis.


Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Arthritis, Experimental/drug therapy , Arthritis, Rheumatoid/drug therapy , Neutrophils/drug effects , Phytotherapy , Semecarpus , Animals , Antioxidants/pharmacology , Antirheumatic Agents/pharmacology , Arthritis, Experimental/immunology , Arthritis, Experimental/metabolism , Arthritis, Rheumatoid/immunology , Arthritis, Rheumatoid/metabolism , Free Radicals , Lipid Peroxidation/drug effects , Lipid Peroxidation/physiology , Male , Neutrophils/immunology , Nuts , Phagocytosis/drug effects , Plant Extracts/pharmacology , Rats , Rats, Wistar , Reactive Nitrogen Species/metabolism , Reactive Oxygen Species/metabolism
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