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Session: Personalizing Nutrition - Select Genetic, Epigenetic and Microbiome Interactions Influencing Diet and Diet-related Diseases (Oral 13)

(OR13-06-23) FADS-Associated Risk on Cardiovascular Biomarkers Depends on Circulating Omega-6 Fatty Acids

Sunday, July 23, 2023
5:00 PM – 5:12 PM ET
Location:  Constitution B
GSRA ELPC

    Presenting Author(s)

  • Carmen Annevelink, BA

    Graduate Student
    The Pennsylvania State University
    State College, Pennsylvania, United States

    Disclosure(s): No relevant financial relationship(s) with ineligible companies to disclose.

    • Co-Author(s)

  • GS

    Gregory C. Shearer, PhD

    The Pennsylvania State University
    University Park, Pennsylvania, United States

  • NT

    Nathan L. Tintle, PhD

    Senior Scientist
    Fatty Acid Research Institute
    SIOUX FALLS, South Dakota, United States

  • JW

    Jason Westra

    Fatty Acid Research Institute

Disclosure(s):
Carmen Annevelink, BA: No relevant financial relationship(s) with ineligible companies to disclose.
Objectives: To determine if the FADS-associated risk for cardiovascular disease (CVD) depends on circulating omega-6 fatty acids (N6FA).

Methods: White UK Biobank participants with circulating FA and outcome data at baseline (N = 96,892) were analyzed cross-sectionally. Linear regression models were used to predict six CVD measures: total cholesterol (TC), log(HDL-c), LDL-c, log(CRP), log(HbA1c), and total triglycerides (log(TG)). Health markers using an individual’s fatty acid desaturase (FADS) genotype (DD, Da, aa), with the addition of N6FA measures as additive or interaction (with FADS) terms to test mediation and moderation hypotheses, respectively. Models were adjusted for demographic and medical history variables.

Results: Across 36 tests, we found evidence for 7 moderation effects and 1 partial mediation effect of the FADS-health relationship. All results were highly statistically significant (p < 0.0001), except where noted. Non-LA N6FAs moderate an individual’s HDL-c such that at higher levels of non-LA N6FAs, individuals with minor alleles have significantly lower HDL-c (mmol/L) ((Adjusted diff (95% CI) DD vs Da: -0.024 [-0.03, -0.019]; DD vs aa: -0.055 [-0.066, -0.045])). This effect is not present with LA or total N6FA. There is an interaction of total N6FA and non-LA N6FA with FADS genotypes on LDL-c (mmol/l). For example, LDL-c is only significantly different between genotype groups at the lowest quartile of n6FA (DD vs Da: -0.033 [-0.045, -0.022]; DD vs aa: -0.077 [-0.096, -0.059]), however at higher N6FA there is no significant difference. With increasing non-LA N6FA, all individuals have decreasing LDL-c, however individuals with minor alleles have lower LDL-c at all levels (Q3: DD vs Da: -0.087 [-0.096, -0.077]; DD vs aa: -0.20 [-0.21, -0.18]).

Conclusions: Cross-sectional evidence suggests that individuals with low total N6FA appear to benefit more from having the recessive FADS haplotype. Further, for individuals with the recessive haplotype, there is evidence that higher N6FA appears to be protective from high LDL-c, but when non-LA N6FA are high, these individuals also have low HDL-c.

Funding Sources: NIGMS, NHLBI