Optimal Result: 0 - 0.86 ng/mg.

F2-Isoprostane, prostaglandin-like compounds formed from the free radical-mediated oxidation of arachidonic acid, are the ‘gold standard’ for measuring oxidative stress in the body.

F2-Isoprostane also have potent biological effects associated with inflammation and therefore may mediate chronic disease initiation and progression.

Additionally, F2-Isoprostane may also act as potent vasoconstrictors via thromboxane formation in the endothelium and promote platelet activation resulting in thrombus formation.

The F2-Isoprostane test may be performed on individuals at risk of future cardiovascular disease due to lifestyle risks, or those with a family history of cardiovascular disease.

Testing of F2 -Isoprostanes is determined by an individual’s medical history, but may be performed semi-annually or annually as necessary. If the initial test result is abnormal, then follow-up testing may be performed within 3-6 months following treatment.


- Morrow JD et al. Quantification of Isoprostanes as Indices of oxidant Stress and the Risk of Atherosclerosis in Humans. Arterioscler Thromb Vasc Biol. 2005;25:279-286.

- Morrow JD et al. The F2-isoprostane, 8-epi-prostaglandin F2alpha, a potent agonist of the vascular thromboxane/endoperoxide receptor, is a platelet thromboxane/endoperoxide receptor antagonist. Prostaglandins. 1992; 44: 155-163.

- Minuz P et al. The F2-isoprostane 8-epiprostaglandin F2alpha increases platelet adhesion and reduces the antiadhesive and antiaggregatory effects of NO. Arterioscler Thromb Vasc Biol. 1998; 18: 1248-1256.

- Schwedhelm E et al. Urinary 8-iso-prostaglandin F2alpha as a risk marker in patients with coronary heart disease: A matched case-control study. Circulation. 2004; 109: 843-848.

- Rossner P Jr et al. Relationship between urinary 15-F2t-isoprostane and 8-oxodeoxyguanosine levels and breast cancer risk. Cancer Epidemiol Biomarkers Prev. 2006; 15: 639-644.

- Epplein M et al. Association of plasma micronutrientlevelsandurinaryisoprostanewithriskoflungcancer:Themultiethniccohortstudy.CancerEpidemiolBiomarkersPrev.2009;18:1962-1970.

- MorrowJDetal.Increaseincirculatingproducts of lipid peroxidation (F2-Isoprostanes) in smokers. Smoking as a cause of oxidative damage. N Engl J Med. 1995; 332: 1198-1203.

- Tappel A. Heme of consumed red meat can act as a catalyst of oxidative damage and could initiate colon, breast and prostate cancers, heart disease and other diseases. Med Hypotheses.2007; 68: 562-564.

- Keaney JF et al. Obesity and Systemic Oxidative Stress. Arterioscler Thromb Vasc Biol. 2003;23:434-439.

- Davi G et al. Platelet activation in obese women: role of inflammation and oxidant stress. JAMA. 2002;288(16):2008-14.

- Shi M et al. Effects of anaerobic exercise and aerobic exercise on biomarkers of oxidative stress. Environ Health Prev Med. 2007;

- 202-208. 12. Nikolaidis MG et al. F2-Isoprostane formation, measurement and interpretation: The role of exercise. Prog in Lipid Res. 2010;50:89-103.

- Watson TA et al. Antioxidant Restriction and Oxidative Stress in Short Duration Exhaustive Exercise. Med Sci Sports Exerc. 2005; 37(1):63-71.

- Mas E et al. The omega-3 fatty acids EPA and DHA decrease plasma F2-Isoprostanes: Results from two placebo-controlled interventions. Free Radical Research. 2010;44(9):983-90.

- Minuz P et al. The F2-Isoprostane 8-Epiprostaglandin F2α Increases Platelet Adhesion and Reduces the Antiadhesive and Antiaggregatory Effects of NO. Arterioscler Thromb Vasc Biol. 1998;18:1248-1256.

What does it mean if your F2-Isoprostane result is too high?

Elevated urinary F2-isoprostanes reflect widespread oxidative stress and systemic burden of lipid peroxidation end products. 

F2-Isoprostane levels are increased with:

- Cigarette smoking

- Poor diet (including high red meat intake)

- Sedentary lifestyle

- Elevated levels of urinary F2-Isoprostane are seen in conditions associated with increased risk for atherosclerosis and certain forms of cancer.

Treatment Considerations:

These treatment considerations are for educational purposes only. Specific treatment plans should be provided and reviewed by the treating practitioner.

Assess smoking habits:

Smoking cessation is essential as individuals who smoke are at increased risk of heart disease and blood clots.

Assess lifestyle habits:

- Consider diet, weight reduction, aerobic and anaerobic exercise, as appropriate.

- Consider optimal caloric intake as individuals who exercise a lot may not be taking in enough calories for their activity level. In short, they may be at risk for increased oxidation in their bodies due to lack of nutritional balance.

Assess omega-3 fatty acid levels:

If not at optimal levels, consider fish oil supplements, other dietary supplements, and dietary recommendations for increasing omega-3 fatty acid levels.

Assess clotting risk:

Consider anti-platelet therapy if history of CAD (i.e., myocardial infarction or revascularization) and/or cerebrovascular disease (i.e., transient ischemic attack or stroke).

Frequently asked questions

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