Abstract
Abdominal aortic aneurysm (AAA) is an important cause of death in older adults, which has no current drug therapy. Inflammation and abnormal redox status are believed to be key pathogenic mechanisms for AAA. In light of evidence correlating inflammation with aberrant fatty acid profiles, this study compared erythrocyte fatty acid content in 43 AAA patients (diameter 3.0-4.5 cm) and 52 healthy controls. In addition, the effect of omega-3 PUFA (n-3 PUFA) supplementation on erythrocyte fatty acid content was examined in a cohort of 30 AAA patients as part of a 12 week randomized placebo-controlled clinical trial. Blood analyses identified associations between AAA and decreased linoleic acid (LA), and AAA and increased Δ6-desaturase activity and biosynthesis of arachidonic acid (AA) from LA. Omega-3 PUFA supplementation (1.5 g DHA + 0.3 g EPA/day) decreased red blood cell distribution width (14.8 ± 0.4% to 13.8 ± 0.2%; P = 0.003) and levels of pro-inflammatory n-6 PUFAs (AA, 12.46 ± 0.23% to 10.14 ± 0.3%, P < 0.001; adrenic acid, 2.12 ± 0.13% to 1.23 ± 0.09%; P < 0.001). In addition, Δ-4 desaturase activity increased (DHA/docosapentaenoic acid ratio, 1.85 ± 0.14 to 3.93 ± 0.17; P < 0.001) and elongase 2/5 activity decreased (adrenic acid/AA ratio, 0.17 ± 0.01 to 0.12 ± 0.01; P < 0.01) following supplementation. The findings suggest that n-3 PUFAs improve fatty acid profiles and ameliorate factors associated with inflammation in AAA patients.
Highlights
Supplementary key words omega-3 fatty acids antioxidants clinical studies diet and dietary lipids diet effects/lipid metabolism abdominal aortic aneurysms omega-3 index polyunsaturated fatty acids
The lower levels of linoleic acid (LA) in conjunction with higher levels of adrenic acid in the Abdominal aortic aneurysm (AAA) cohort are of note
A meta-analysis of prospective cohort studies (n = 310,602 participants, n = 12,479 cases) indicated that the highest levels of dietary LA intake were associated with a 15% lower risk of coronary heart disease (CHD) events and a 21% lower risk of CHD deaths when compared with the lowest levels of LA intake [34]
Summary
Animal data have suggested the potential of n-3 PUFA supplementation to limit small AAA growth through positive impacts on oxidative stress status [6, 7] and interference with inflammatory cascades [8,9,10]. While clinical evidence in AAA patients is limited, low serum EPA levels have been reported to be associated with larger aneurysm size and faster growth rate in a Japanese patient population [11]. J.G. holds a Practitioner Fellowship from the National Health and Medical Research Council (1117061) and a Senior Clinical Research Fellowship from the Queensland Government, Australia. This trial was registered at anzctr.org.au as ANZCTR12616000483459 Manuscript received 4 February 2019 and in revised form 6 March 2019.
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