Abstract
BackgroundAvailable data about the effects of circulating polyunsaturated fatty acids (PUFAs) on ischemic stroke (IS) and its main risk factors remains limited and conflicting. Therefore, we conducted Mendelian randomization (MR) to assess whether genetically predicted PUFA affected IS, lipids and blood pressure (BP).MethodsGenetic instruments associated with IS were derived from ISGC Consortium (n = 29,633), with lipids were derived from GLGC(n = 188,577), with BP were derived from Neale Lab(n = 337,000). The inverse-variance weighted method was the main analysis to estimate the effect of exposure on outcome. Sensitivity analyses included principal components analysis, MR-Egger, weighted median, and weighted mode.ResultsPer SD increases in serum α-linolenic acid (ALA) were associated with lower IS risk, with odd ratio (OR) of 0.867(0.782,0.961), arachidonic acid (AA) were associated with higher IS risk (OR: 1.053(1.014,1.094)). Likewise, Per SD increases in ALA were associated with the lower-level low-density lipoprotein cholesterol(LDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC) (β:-0.122(− 0.144, − 0.101), − 0.159(− 0.182, − 0.135), − 0.148(− 0.171, − 0.126), respectively), AA were associated with the higher-level of LDL-C, HDL-C and TC (β:0.045(0.034,0.056), 0.059(0.050,0.067), 0.055(0.046,0.063), respectively). Linoleic acid (LA), eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and docosapentaenoic acid (DPA) had little or no association with IS, lipids or BP at Bonferroni-corrected significance. Different analytic methods supported these findings. The intercept test of MR-Egger implied no pleiotropy.ConclusionsHigh-level plasma ALA was protective for IS but AA was the opposite. LA, EPA, DHA, and DPA had no effects on IS.
Highlights
Available data about the effects of circulating polyunsaturated fatty acids (PUFAs) on ischemic stroke (IS) and its main risk factors remains limited and conflicting
Genetic instruments associated with IS were derived from International Stroke Genetics Consortium (ISGC) Consortium (n = 29,633), with lipids were derived from Global Lipids Genetic Consortium (GLGC)(n = 188,577), with blood pressure (BP) were derived from Neale Lab(n = 337,000)
Per standard deviation (SD) increases in α-Linolenic acid (ALA) were associated with the lower-level low-density lipoprotein cholesterol(LDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC) (β:-0.122(− 0.144, − 0.101), − 0.159(− 0.182, − 0.135), − 0.148(− 0.171, − 0.126), respectively), arachidonic acid (AA) were associated with the higher-level of Lower-level low-density lipoprotein cholesterol (LDL-C), HDL-C and TC (β:0.045(0.034,0.056), 0.059(0.050,0.067), 0.055(0.046,0.063), respectively)
Summary
Available data about the effects of circulating polyunsaturated fatty acids (PUFAs) on ischemic stroke (IS) and its main risk factors remains limited and conflicting. A systematic assessment involving 17 randomized controlled trials (RCTs) found that stroke might not be affected by omega-6 fatty acids intake [11]. Another meta-analysis including 30 observational studies indicated that increased ingestion of LA was associated with a lower risk of IS risk and AA had no association with the risk of IS [14]. A recent pooled-analysis of 79 RCTs substantiated that long-chain omega-3(EPA, DHA) supplements had no effect on IS, ALA had an unclear effect on stroke [10] These conventional studies were limited by different duration, events, memory bias or confounders, so the evidence was different from each. The estimation of PUFA may be biased by recall bias or measurement error and less precise than directly detect the PUFA concentration in the blood [24]
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