A plant source of omega-3 fatty acid (FA) that can raise tissue eicosapentaenoic acid (EPA) and/or docosahexaenoic acid (DHA) is needed. A soybean oil (SBO) containing approximately 20% stearidonic acid [SDA; the delta-6 desaturase product of alpha-linolenic acid (ALA)] derived from genetically modified soybeans is under development. This study compared the effects of EPA to SDA-SBO on erythrocyte EPA+DHA levels (the omega-3 index). Overweight healthy volunteers (n=45) were randomized to SDA-SBO (24 ml/day providing approximately 3.7 g SDA) or to regular SBO (control group) without or with EPA ethyl esters (approximately 1 g/day) for 16 weeks. Serum lipids, blood pressure, heart rate, platelet function and safety laboratory tests were measured along with the omega-3 index. A per-protocol analysis was conducted on 33 subjects (11 per group). Compared to baseline, average omega-3 index levels increased 19.5% in the SDA group and 25.4% in the EPA group (p<0.05 for both, vs. control). DHA did not change in any group. Relative to EPA, SDA increased RBC EPA with about 17% efficiency. No other clinical endpoints were affected by SDA or EPA treatment (vs. control). In conclusion, SDA-enriched SBO significantly raised the omega-3 index. Since EPA supplementation has been shown to raise the omega-3 index and to lower risk for cardiac events, SDA-SBO may be a viable plant-based alternative for providing meaningful intakes of cardioprotective omega-3 FAs.

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The metabolic syndrome includes both dyslipidemia and impaired vascular function. Because extended-release niacin (ERN) and prescription omega-3 acid ethyl-esters (P-OM3) independently improve these characteristics, we tested their effects in combination. Sixty metabolic syndrome subjects were randomized to 16 weeks of treatment on dual placebo, P-OM3 (4g/day), ERN (2 g/day), or combination in a double-blind trial. Lipoprotein subfractions and vascular endpoints were measured and tested using ANCOVA. ERN increased HDL cholesterol by 5.4 mg/dl from baseline (P = 0.04), decreased triglycerides (TG) by 39 mg/dl (−21%, P = 0.003), and decreased the augmentation index, which is a measure of vascular stiffness, by 3.5 units (P = 0.04). P-OM3 reduced TG by 26 mg/dl (−13%, P = 0.04). Combination treatment increased HDL cholesterol by 7.8 mg/dl (P = 002) and decreased TG by 72 mg/dl (−34%) but there was no improvement in vascular stiffness. Detailed analysis of lipoprotein subfractions revealed increased large, bouyant HDL2 (3.3 mg/dl; P = 0.002) and decreased VLDL1+2 (−32%; P < 0.0001), among subjects treated with combination therapy, that were not present with either therapy alone. ERN and P-OM3 alone improved characteristics of metabolic syndrome; however, whereas subjects on combination therapy did not have improved vascular stiffness, TG and HDL levels improved as did certain lipoprotein subfractions.

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The role of long chain omega-3 fatty acids (LC n-3 FAs) as cardioprotective agents has become even clearer with the recent publication of the Japan EPA Lipid Intervention Study. This was the largest randomized controlled trial in the field, and it demonstrated that even in a population with one of the highest LC n-3 FA intakes in the world, the addition of eicosapentaenoic acid could reduce cardiac events. A comprehensive analysis of the risks and benefits of fish consumption was likewise recently published that should quiet any remaining fears that there are substantial risks to consuming oily fish such as salmon. A new meta-analysis has now demonstrated that reduced tissue/blood levels of LC n-3 FAs provide a better indication of increased cardiovascular risk than the n-6:n-3 ratio. Finally, a supplementation study in cardiac surgery patients has demonstrated both the time course and extent of incorporation of LC n-3 FAs into the human heart.

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We evaluated the effects of 2 h of warm (24°C) and cold (6°C) exposure on metabolism and ventilation (v̇_E) in conscious male and female Harlan ICR Swiss Webster mice exposed to air, and 8% O₂ in N₂ (hypoxia) and to 5% CO₂ in O₂ (hypercapnia) for 2 min each at both temperatures. All cold-exposed mice increased O₂ consumption (v̇_O2), and maintained body temperature. Cold-exposed females doubled their tidal volume, increased their v̇_E fivefold, and doubled their ventilatory equivalent to v̇_O2 (v̇_E/v̇_O2). In contrast, cold-exposed males decreased tidal volume and doubled v̇_E relative to warm exposure. The ventilatory equivalent of males was similar during warm and cold exposure. During warm exposure, mice of both genders increased their ventilatory responses to both hypoxia and to hypercapnia by different mechanisms. In contrast, during cold exposure, these responses were blunted relative to air measurements in females and decreased below air values in males. Thus, cold exposure was able to elicit gender-specific ventilatory and metabolic responses.

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