High-dose omega-3 fatty acids have no effect on platelet aggregation or coagulation measured with static and flow-based aggregation instruments and Sonoclot; an observational study in healthy volunteers

Bagge, August; Schött, Ulf; Kander, Thomas

doi:10.1080/00365513.2018.1516477

Cited by 13 publications

(12 citation statements)

References 32 publications

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“…Some scholars believe that the risk of theoretical adverse effects of excessive bleeding did not exist, and current evidence suggests that under concurrent usage of antiplatelet or anticoagulant agents, doses up to 4 g of n-3 PUFAs daily are not associated with an increased risk of major bleeding [27]. An observation on healthy volunteers revealed that high-dose n-3 PUFAs (2520 mg) has no effect on platelet aggregation or coagulation measured with static and flow-based aggregation instruments and Sonoclot [28]. Recently, Guidelines also indicate that the theoretical risk of excessive bleeding from n-3 PUFAs does not exist, even if patients are using antiplatelet and anticoagulants [12].…”

Section: Discussionmentioning

confidence: 99%

High-dose omega-3 polyunsaturated fatty acid supplementation might be more superior than low-dose for major depressive disorder in early therapy period: a network meta-analysis

et al. 2020

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Background: The application of n-3 Polyunsaturated Fatty Acids (n-3 PUFAs) supplementation for major depressive disorder (MDD) has been widely discussed in recent years, but its efficacy and application are still controversial. This network meta-analysis was conducted to compare the efficacy of different dosages of n-3 PUFAs on MDD patients in the early period of treatment. Methods: Randomized controlled trials (RCTs) exploring the efficacy of n-3 PUFA supplementation for patients with MDD were retrieved from the databases of Pubmed, Embase and the Cochrane Library. RCTs comparing the efficacy of n-3 PUFA for adult (≥18 years) MDD patients without comorbidity were eligible for our study. The score of depressive symptoms in early therapy period of the treatment (≤9 weeks) was extracted. Standardized mean deviations (SMDs) of all the sores from the eligible RCTs were synthesized in a pairwise meta-analysis in frequentist framework and a random-effects network meta-analysis in Bayesian framework for the overall and subgroups (highand low-dose) efficacy of n-3 PUFAs. Results: A total of 910 MDD patients in 10 trials with 3 adjuvant therapy strategies (high-dose n-3 PUFAs, low-dose n-3 PUFAs and placebo) were included. Results of pairwise meta-analysis showed that n-3 PUFAs were superior to placebo (SMD: 1.243 ± 0.596; 95% CI: 0.060~2.414). Results of the network meta-analysis showed that both the high (SMD: 0.908 ± 0.331; 95% CI: 0.262~1.581) and the low-dose (SMD: 0.601 ± 0.286; 95% CI: 0.034~1.18) n-3 PUFAs were superior to placebo, and the efficacy of high-dose n-3 PUFAs is superior to that of low-dose. Conclusions: High-dose n-3 PUFAs supplementation might be more superior than low-dose in the early therapy period for MDD. More head-to-head clinical trials need to be carried out to provide more direct comparison and enhance the evidence of the efficacy of n-3PUFAs for MDD.

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Section: Discussionmentioning

confidence: 99%

High-dose omega-3 polyunsaturated fatty acid supplementation might be more superior than low-dose for major depressive disorder in early therapy period: a network meta-analysis

et al. 2020

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“…Bagge et al [26] found a significant change in MEA ADP AUC following 7 days of daily 1260 mg Omega-3 ingestion in a prospective pilot study. However, in a follow-up study with 10 days of daily 2520 mg ingestion, no significant results were found [48]. While Cao et al did not use MEA (unlike Bagge et al), the far more direct method of measuring Omega-3 levels used by Cao et al make their study more relevant in terms of discussing adequate Omega-3 treatment period for future studies.…”

Section: Discussionmentioning

confidence: 94%

“…Omega-3 can reduce the von Willebrand factor (shear dependant platelet activator) [47]. We have previously studied Omega-3 effects with an automatic flow chamber technique (Cellix™) with high shear stress, but failed to detect any platelet inhibiting effect [48]. Cohen et al used electrophoretic quasi-elastic light scattering technology (EQELS) technology to study Omega-3 effects and found an increased negative resting platelet charge, e.g.…”

Section: Discussionmentioning

confidence: 99%

Synergistic platelet inhibition between Omega-3 and acetylsalicylic acid dose titration; an observational study

Bagger

Hansson

Kander

et al. 2020

BMC Complement Med Ther

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Background: Omega-3 and acetylsalicylic acid (ASA) are two widely used "over-the-counter" drugs. Previous research has shown multiple electrode aggregometry (MEA) can detect ASA and varying Omega-3 platelet inhibiting effects. Synergistic platelet inhibiting effects of ASA and Omega-3 have been found using other methods than MEA. The aim of this study was to investigate the antiplatelet effects of Omega-3, and ASA synergism with MEA. Methods: Ten healthy male volunteers ingested Omega-3 (1260 mg/day) for 5 days. MEA was used to analyse platelet function before and after Omega-3 intake. Aggregation was initiated using three different agonists and measured as area under the curve (AUC): adenosine diphosphate (ADP), thrombin receptor activating peptide (TRAP) and arachidonic acid (ASPI). Two concentrations of ASA were dose titrated ex vivo to 2 out of 3 ASPI test cells in order to measure synergism between Omega-3 and ASA. Results: Following 5 days Omega-3 intake, ADP, TRAP and ASPI AUC did not change significantly. In vitro ASA before Omega-3 intake, reduced ASPI AUC < 30 U, indicating a strong platelet inhibiting effect. Below this AUC level, the 5 days Omega-3 intake increased ASPI-AUC with the ex vivo added low dose ASA (P = 0.02) and high dose ASA (P = 0.04). Conclusions: No synergism between ASA and Omega-3 was found using the MEA ASPI test. The surprising increase in ASPI-AUC following Omega-3 intake and ex vivo ASA suggest that there are methodological issuses with the MEA ASPI test. Trial registration: Trial registration ISRCTN78027929. Registered 19 May 2015.

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“…To measure clot formation and strength as well as the interaction between platelet and fibrin, a Sonoclot Coagulation Analyzer, a viscoelastic test instrument, was used with a glass bead test (Sienco 1 gbACT™ Kit) [39]. Citrated blood was re-calcified moments prior to the test assays to reverse the citrate's anticoagulant effect.…”

Section: Sonoclot Coagulation Analyzermentioning

confidence: 99%

“…The following variables were measured, with the defined normal values in parentheses: Activated clotting time (ACT) (100−155 s) is the time required for the first fibrin to form. Clot rate (CR) (9−35 units/min) is the rate of increase in the clot impedance due to fibrin formation and polymerization [39].…”

Section: Sonoclot Coagulation Analyzermentioning

confidence: 99%

Intense light as anticoagulant therapy in humans

et al. 2020

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Blood coagulation is central to myocardial ischemia and reperfusion (IR) injury. Studies on the light elicited circadian rhythm protein Period 2 (PER2) using whole body Per2-/- mice found deficient platelet function and reduced clotting which would be expected to protect from myocardial IR-injury. In contrast, intense light induction of PER2 protected from myocardial IR-injury while Per2 deficiency was detrimental. Based on these conflicting data, we sought to evaluate the role of platelet specific PER2 in coagulation and myocardial ischemia and reperfusion injury. We demonstrated that platelets from mice with tissue-specific deletion of Per2 in the megakaryocyte lineage (Per2loxP/loxP-PF4-CRE) significantly clot faster than platelets from control mice. We further found increases in infarct sizes or plasma troponin levels in Per2loxP/loxP-PF4-CRE mice when compared to controls. As intense light increases PER2 protein in human tissues, we also performed translational studies and tested the effects of intense light therapy on coagulation in healthy human subjects. Our human studies revealed that intense light therapy repressed procoagulant pathways in human plasma samples and significantly reduced the clot rate. Based on these results we conclude that intense light elicited PER2 has an inhibitory function on platelet aggregation in mice. Further, we suggest intense light as a novel therapy to prevent or treat clotting in a clinical setting.

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High-dose omega-3 fatty acids have no effect on platelet aggregation or coagulation measured with static and flow-based aggregation instruments and Sonoclot; an observational study in healthy volunteers

Cited by 13 publications

References 32 publications

High-dose omega-3 polyunsaturated fatty acid supplementation might be more superior than low-dose for major depressive disorder in early therapy period: a network meta-analysis

High-dose omega-3 polyunsaturated fatty acid supplementation might be more superior than low-dose for major depressive disorder in early therapy period: a network meta-analysis

Synergistic platelet inhibition between Omega-3 and acetylsalicylic acid dose titration; an observational study

Intense light as anticoagulant therapy in humans

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