Can Omega 3s Cause Nosebleeds?

Nov 18, 2021 | General, Nutrition | 0 comments

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Yes! Omega 3 Supplements Can Cause Nose Bleeds

Omega 3 supplements can increase the likelihood and frequency of nose bleeds (epistaxis). It is thought that the anti-platelet activity of omega 3 fatty acids leads to a reduced effectiveness of blood clotting. In individuals with dysfunctional or impaired platelet function, omega 3 supplementation can exacerbate this issue, generating the side effect of an increased bleeding risk which can present in the form of nose bleeds.

Omega 3 supplements are one of the most popular and widely used food supplements on the market, with many different forms available. Regardless of the source, some people notice that they become more prone to bleeding upon taking them. This often occurs in the form of nose bleeds. This is a side effect that does not seem to have an impact on everyone, but nevertheless a significant percentage of the population do experience this side effect.

Why do Omega 3s cause nose bleeds? At first there does not seem to be an obvious connection, but let’s have a look at the possible reasons for this strange side effect. To understand this side effect, we first need to understand the role of platelets and blood clotting.

Platelets And Their Function

Platelets are tiny cells that circulate in the blood of mammals. Platelets are generated from nucleated precursor cells known as ‘megakaryocytes‘ in the bone marrow and lungs, [1] before entering the bloodstream without a nuclei. The cells have little arm-like protrusions called pseudopodia. [2]

An illustration of platelets forming a bundled clot on the side of a blood vessel.
Platelets Are The Building Material Used For Repairing Blood Vessel Damage

The primary function of platelets is to help blood to clot and stop bleeding from wounds. Platelets flow through the blood and the various blood-vessels in a non-active state. In this non-active state, they are shaped like smooth disks, and they are not adhesive.

This inactivated state is to avoid unwanted blood clotting and coagulation, and so instead, the cells travel through blood awaiting activation. Platelets can be activated by injury, infection, or changes to normal blood flow.

Despite their small size, platelets are sensitive to certain chemical indicators, and they are able to respond to a variety of biological changes through receptor sites on their surface. When there is damage to the endothelium, substances are released in to the blood that serve to signal the injury to the platelets in the circulating blood.

Three of these signalling substances are Collagen (in particular, collagen types I, III, and VI), Thrombin and Adenosine diphosphate (ADP).

These substances activate platelets through the receptors on the surface of the platelet cell. This activation results in shape change to the platelet, making it more spherical in shape and extending it’s pseudopodia (those arm-like protrusions). This process makes the cells much stickier, and now they are primed for action. [3] [4]

These activated platelets can now begin to repair the damage, and undergo a process whereby they “rapidly decelerate, roll on the injured endothelium, and firmly adhere.” [5]

A diagram outlining how activated platelets are held together by fibrin to create a clot.
Activated Platelets Are Held Together By Fibrin To Create A Clot

The platelets adhere to the wound with the help of a glycoprotein called the von Willebrand factor (vWF), and a glycoprotein-complex called Fibrinogen. These molecules act as anchors to allow the platelets to adhere to the wall of the blood-vessel. [6]

This is the begining of the formation of a ‘Platelet Plug’. From here, the platelets chemically interact with one another, and the enzyme Thrombin now triggers the Von Willebrand Factor and Fibrinogen to begin binding the platelets together. This process is called ‘Platelet Aggregation‘.

Activated platelets produce a substance called ‘Thromboxane A2‘, a signalling chemical that helps to activate more platelets and further increase platelet aggregation. Platelets have ‘Thromboxane receptors’ on their surface, and Thomboxane A2 binds to these receptors, activating the platelet. Fibrinogen also binds these receptors, using them as points to connect platelets together. [7]

ADP is also used in this process, and catalyses the aggregation, attracting and activating more platelets in a positive feedback loop. Once this process has gone on long enough, the wound is blocked with a mass of platelets held together with Fibrinogen, and this completes the first stage of the plug formation.

Now the Secondary stage can begin, and Thrombin now converts the Fibrinogen, which is soluble, in to the glycoprotein Fibrin, which is insoluble. This begins to harden the plug and give it greater strength and rigidity. The fibrin acts like a mesh of threads, holding the cells in place. [8]

Finally, the process is consolidated with a substance called ‘Factor XIII‘. This substance consolidates the plug by cross-linking the fibrin, hardening the mesh. The platelet plug is now complete, and the bleeding stops.

Omega 3s & Platelet Disruption

Omega 3 fatty acids are Alpha-Linolenic Acid (ALA), Docosahexaenoic Acid (DHA) and Eicosapentaenoic Acid (EPA). Once consumed, ALA is converted in the body in to DHA and EPA, but the process is very inefficient. For this reason, Omega 3 supplementation focuses on DHA and EPA mainly.

A photo of Omega 3 supplement capsules, which provide both DHA & EPA.
Omega 3 Capsules Provide Both DHA & EPA

In a study by C. von Schacky & P. C. Weber, it was found that “ingestion of both EPA and DHA resulted in reduced platelet aggregation in response to collagen.” [9]

Furthermore, DHA lowered the platelets response to ADP. [9] As we discussed in our section above, ADP is used both in the signalling process to the platelets, and also as a catalyst in the formation of the plug. Platelets that are desensitised to ADP are therefore going to be less reactive to the initial stimuli of the wound, and this desensitisation could slow down the platelet plug formation.

This study also found that there was a delayed effect from the ingestion of Omega 3s before the effect began to show up in the blood. EPA was found in blood plasma after four hours, but was not found in platelet composition until six days after ingestion. [9]

A possible mechanism for this is that the alterations to the platelets was occurring during their development in the megakaryocytes.

The practical implications of this have been studied by evaluating ‘bleeding duration’ in controlled settings. A 2011 study found that “Mean bleeding time increased in a dose-dependent manner with escalating omega-3 doses.” [10] This study concluded that Omega 3 ingestion increased the total platelet surface charge, and therefore, attenuated platelet activation.

Omega 3s not only seem to reduce platelet activation, but also also have an effect on lowering platelet aggregation as well. Research has found that omega 3s diminish Thromboxane A2 production by platelet membranes, which would lead to both a lower rate of activation and aggregation. As we discussed above, Thromboxane A2 is a crucial chemical signaller that helps activate and attract more platelets to the growing plug. [11]

A case study was conducted on a Johns Hopkins Hospital patient who presented excessive bleeding from Omega 3 consumption. The researches found evidence that ‘impaired platelet function’ was behind the effect.

“Some patients may be more susceptible to the platelet-aggregation reduction effect of fish oils than others; the patient in our case clearly had evidence of impaired platelet function and objectively diminished platelet function.”

Adam R. Berliner, Derek M. Fine – There’s Something Fishy About This Bleeding. NDT Plus, Volume 4, Issue 4, August 2011, Pages 270–272 [12]

Very large doses of Omega-3 ingestion in healthy volunteers at doses of 13.8 g daily can alter the balance between pro-thrombotic and anti-thrombotic eicosanoids in favour of an anti-thrombotic state. This dosage is a lot higher than average consumption. [13]

The effect that omega 3 fatty acids have on platelets and blood clotting are not limited just to high doses of supplement intake. One study even used autopsy data to look at a potential connection to high dietary intake in fishing communities of Greenland, and an increase of haemorrhagic stroke in these populations. [14] However, when consumed by healthy individuals and sticking to moderate, recommended doses, Omega 3s are deemed to be very safe, and are not generally linked to excessive bleeding risks under normal conditions. [15]

Clearly, there are lots of factors to take in to account when asking why Omega 3s could cause nose bleeds. The individuals baseline platelet function, the propensity to get nose bleeds ordinarily, and the dosage of Omega 3 intake are all factors to consider when talking about this side effect.

Conclusion

It has been shown that high dietary omega-3 fatty acid intake causes changes in the fatty acid composition of platelet membranes, and leads to a reduction of platelet aggregation and thrombogenesis. [16] Furthermore, the effect seems to be dose dependent, with higher doses leading to a more pronounced effect.

Omega 3 supplementation can disrupt platelet function, potentially leading to increased risk of bleeding, including in the form of nose bleeds. Omega 3 nosebeeds are likely the result of platelet dysfunction.

However, the effect does not seem to be pronounced in healthy individuals with normal platelet function. Individuals who are sensitive to platelet disruption, or are already operating from a baseline of platelet dis-regularity are most likely to experience nosebleeds in relation to Omega 3 intake. Furthermore, this side effect often ceases when Omega 3 intake is reduced or stopped.

Finally, due to the effect Omega 3s have on reducing platelet activation and aggregation, it is sensible to take care with omega 3 ingestion if you are on any other medications that interfere with platelet function. These medications include Aspirin, Ibuprofen, and pharmaceutical blood thinning medications.

Consult with your doctor if you are concerned about Omega 3 intake, or any of the issues addressed in this article.

[References]

1. Lefrançais E, Ortiz-Muñoz G, Caudrillier A, Mallavia B, Liu F, Sayah DM, Thornton EE, Headley MB, David T, Coughlin SR, Krummel MF, Leavitt AD, Passegué E, Looney MR. The lung is a site of platelet biogenesis and a reservoir for haematopoietic progenitors. Nature. 2017 Apr 6;544(7648):105-109. doi: 10.1038/nature21706. Epub 2017 Mar 22. PMID: 28329764; PMCID: PMC5663284.

2. Italiano JE Jr, Lecine P, Shivdasani RA, Hartwig JH. Blood platelets are assembled principally at the ends of proplatelet processes produced by differentiated megakaryocytes. J Cell Biol. 1999 Dec 13;147(6):1299-312. doi: 10.1083/jcb.147.6.1299. PMID: 10601342; PMCID: PMC2168104.

3. Molecular Basis for ADP-induced Platelet Activation, Evidence For Three Distinct ADP Receptors On Human Platelets, CELL BIOLOGY AND METABOLISM| VOLUME 273, ISSUE 4, P2024-2029, JANUARY 1998

4. Aslan JE, Itakura A, Gertz JM, McCarty OJ. Platelet shape change and spreading. Methods Mol Biol. 2012;788:91-100. doi: 10.1007/978-1-61779-307-3_7. PMID: 22130702.

5. Rajinder N. Puri, Robert W. Colman & Dr. Michael A. Liberman (2008) ADP-lnduced Platelet Activation, Critical Reviews in Biochemistry and Molecular Biology, 32:6, 437-502, DOI: 10.3109/10409239709082000

6. Yun SH, Sim EH, Goh RY, Park JI, Han JY. Platelet Activation: The Mechanisms and Potential Biomarkers. Biomed Res Int. 2016;2016:9060143. doi: 10.1155/2016/9060143. Epub 2016 Jun 15. PMID: 27403440; PMCID: PMC4925965.

7. Offermanns S. Activation of platelet function through G protein-coupled receptors. Circ Res. 2006 Dec 8;99(12):1293-304. doi: 10.1161/01.RES.0000251742.71301.16. PMID: 17158345.

8. Hawiger J. Formation and regulation of platelet and fibrin hemostatic plug. Hum Pathol. 1987 Feb;18(2):111-22. doi: 10.1016/s0046-8177(87)80330-1. PMID: 3804319.

9. von Schacky C, Weber PC. Metabolism and effects on platelet function of the purified eicosapentaenoic and docosahexaenoic acids in humans. J Clin Invest. 1985 Dec;76(6):2446-50. doi: 10.1172/JCI112261. PMID: 3001149; PMCID: PMC424407.

10. Cohen MG, Rossi JS, Garbarino J, Bowling R, Motsinger-Reif AA, Schuler C, Dupont AG, Gabriel D. Insights into the inhibition of platelet activation by omega-3 polyunsaturated fatty acids: beyond aspirin and clopidogrel. Thromb Res. 2011 Oct;128(4):335-40. doi: 10.1016/j.thromres.2011.04.023. Epub 2011 May 28. PMID: 21621252.

11. Adam R. Berliner, Derek M. Fine, There’s something fishy about this bleeding, NDT Plus, Volume 4, Issue 4, August 2011, Pages 270–272, https://doi.org/10.1093/ndtplus/sfr046

12. Engström K, Wallin R, Saldeen T. Effect of low-dose aspirin in combination with stable fish oil on whole blood production of eicosanoids. Prostaglandins Leukot Essent Fatty Acids. 2001 Jun;64(6):291-7. doi: 10.1054/plef.2001.0275. PMID: 11427037.

13. Thorngren M, Gustafson A. Effects of 11-week increases in dietary eicosapentaenoic acid on bleeding time, lipids, and platelet aggregation. Lancet. 1981 Nov 28;2(8257):1190-3. doi: 10.1016/s0140-6736(81)91436-7. PMID: 6118628.

14. Pedersen HS,  Mulvad G,  Seidelin KN, et al. N-3 fatty acids as a risk factor for haemorrhagic stroke, Lancet, 1999, vol. 353 (pg. 812-813)

15. Begtrup KM, Krag AE, Hvas AM. No impact of fish oil supplements on bleeding risk: a systematic review. Dan Med J. 2017 May;64(5):A5366. PMID: 28552094.

16. Increased incidence of epistaxis in adolescents with familial hypercholesterolemia treated with fish oil, The Journal of Pediatrics Volume 116, Issue 1, January 1990, Pages 139-141

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Written by Keymer Health

November 18, 2021

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