The effect of fish oils, rich in docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), on eicosanoid production in vivo has been extensively studied, but data on the effects of dietary DHA alone on the synthesis of thromboxane (TXA2) and prostacyclin (PGI2) in humans are lacking.

We quantified the effect of an isocaloric shift in DHA intake from trace (low-DHA diet) to about 6% of total fatty acids (high-DHA diet), ca. 2 en%, on the excretion of 11-dehydrothromboxane B2 (11-DTXB2) and 2, 3-dinor-6-oxo-prostaglandin F1α (PGI2-M). In a longitudinal study, seven healthy men, living in a metabolic unit, were fed a 30% fat low-DHA diet for 30 days, then a high-DHA diet containing 6g/day of DHA for 90 days.

A control group of four subjects remained on the low-DHA diet for the duration of the study (120 days). Three-day urine pools were collected at the end of each dietary period (around day 30 and day 120) and analyzed for eicosanoids by gas chromatography-electron capture negative ion-tandem mass spectrometry.

Mean excretion of 11-DTXB2 was 590 ± 256 ng/d (SD; n = 7) with the low-DHA diet, and 385 ± 148 ng/d (n = 7) with the high-DHA diet, a 35% reduction (p = 0.013, n = 11 including the control group, when log transformed data were used). Production of 11-DTXB2 in the control group was unchanged. Mean excretion of PGI2-M was 229 ± 73 ng/day (SD; n = 7) and 210 ± 102 ng/day with the low-DHA and the high DHA diet, respectively (a nonsignificant reduction).

This study confirms that the synthesis of TXA2 is more open to diet-induced modulation than the synthesis of PGI2. The observed reduction of 11-DTXB2 excretion may be associated with measurable effects on several physiologically significant cellular functions, such as platelet aggregation in vivo and inflammation in response to immune challenges.