Increasing intakes of the long‐chain ω‐3 docosahexaenoic acid: effects on platelet functions and redox status in healthy men

Abstract

Docosahexaenoic acid (DHA) can prevent cardiovascular events. However, few studies have addressed the effects of DHA on both platelet reactivity and redox status in healthy subjects, and dose-related studies are scarce. The main objectives of the present study were to determine the effects of increasing doses of DHA on platelets and redox status in humans. Twelve healthy male volunteers (aged 53-65 yr) were assigned to consume an intake of successively 200, 400, 800, and 1600 mg/d DHA, as the only omega-3 fatty acid, for 2 wk each dose. Blood and urine samples were collected before and after each dose of DHA and at 8 wk after arrest of supplementation. DHA was incorporated in a dose-response fashion in platelet phospholipids. After supplementation with 400 and 800 mg/d DHA, platelet reactivity was significantly decreased. Platelet vitamin E concentration increased only after 200 mg/d DHA, while p38 MAP kinase phosphorylation decreased. Urinary isoprostane was also significantly lowered after 200 mg/d DHA but was increased after 1600 mg/d. Therefore, supplementation with only 200 mg/d DHA for 2 wk induced an antioxidant effect. It is concluded that low consumption of DHA could be an effective and nonpharmacological way to protect healthy men from platelet-related cardiovascular events.

Dose-effect and metabolism of docosahexaenoic acid: Pathophysiological relevance in blood platelets

“…Moreover, monocytes from the volunteers were also more resistant to oxidized LDL-induced apoptosis, especially after the middle dose of DHA (22). Finally, the overall marker of lipid peroxidation, the isoprostane 8-epi-PGF 2α in urine, was significantly lower and higher after 200 mg/day and 1600 mg/day, respectively (20). The decrease of the generated leukotriene (LT) B 4 in calcium ionophore-stimulated PMNs was compensated by LTB 5 , which is known to be much less proinflammatory than LTB 4 (23), and this was proportional to the intake of DHA (24).…”

“…Collagen-induced platelet aggregation was significantly inhibited after 400, 800 and 1600 mg/day but the extent of inhibition was lower at the highest dose. Platelet vitamin E was significantly increased after the lowest dose, while it was increased in low-density lipoproteins (LDL) after the three lowest doses but not after the highest, with a reciprocal decrease of MDA (20,21). In addition, LDL were significantly more resistant to copper-induced oxidation after the same lowest doses.…”

The differential effects of EPA and DHA on cardiovascular risk factors

“…More recently, 8-week supplementation with DHA alone were shown to reduce platelet aggregation to collagen in healthy males for doses as low as 0 . 4 g/d (175) . Due to great variability in terms of design, dose of fish oils and population type, there is inconsistency regarding the effect of fish oils on haemostatic factors in human subjects (151,176) .…”

Dietary α-linolenic acid increases the platelet count in ApoE−/− mice by reducing clearance

“…[1][2][3][4][5][6] Long-chain omega-3 fatty acids (LCn3-FAs) exert beneficial cardiovascular effects on atherosclerosis and inflammation and have been demonstrated to induce antithrombotic and antiplatelet effects and to reduce mortality. [7][8][9][10][11][12][13] Although the Alpha Omega Trial did not show a significantly different event rate among patients receiving LCn3-FA in addition to state-of-the-art therapy for myocardial infarction, 14 previous studies and subgroup analyses demonstrated a beneficial effect of omega (v)-3 FA. 11,15 An inexpensive and abundantly available alternative to marine-derived v-3 is the plant-derived alpha (a)-linolenic acid (ALA) that, by itself or by chain elongation to LCn3-FA EPA, DPA, and DHA, has a number of beneficial effects.…”