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Marie Standl Helmholtz Zentrum München Institute of Epidemiology I

FADS1 FADS2 gene cluster, PUFA intake and blood lipids in children. Results from the GINIplus and LISAplus studies. Marie Standl Helmholtz Zentrum München Institute of Epidemiology I. Bristol, 18/10/11. Background. Dietary PUFA intake. Total cholesterol High-density lipoprotein (HDL)

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Marie Standl Helmholtz Zentrum München Institute of Epidemiology I

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  1. FADS1 FADS2 gene cluster, PUFA intake and blood lipids in children. Results from the GINIplus and LISAplus studies. Marie Standl Helmholtz Zentrum München Institute of Epidemiology I Bristol, 18/10/11

  2. Background Dietary PUFA intake • Total cholesterol • High-density lipoprotein (HDL) • Low-density lipoprotein (LDL) • Triglycerides Cardiovascular diseases FADS Genes

  3. Fatty acid metabolism Omega 6 fatty acid Omega 3 fatty acid Major allele Minor allele FADS Genes More substrate AA (Arachidonic acid) DHA (Docosahexaenoic acid) “pro inflammatory” “beneficial effects” More product

  4. Background Dietary PUFA intake • Total cholesterol • High-density lipoprotein (HDL) • Low-density lipoprotein (LDL) • Triglycerides Cardiovascular diseases Minor allele: Total cholesterol, HDL, LDL Triglycerides FADS Genes

  5. Background Dietary PUFA intake • Objective • Are lipid levels already determined by the FADS genotype in school-aged children? • Interaction between dietary PUFA intake and FADS genotype? • Total cholesterol • High-density lipoprotein (HDL) • Low-density lipoprotein (LDL) • Triglycerides FADS Genes

  6. Methods • Dietary n3 PUFA intake: • Derived from FFQ (food frequency questionnaire) • n3 PUFA = (ALA+EPA+DPA+DHA)/total dietary energy intake • Results presented as mg/MJ per interquartile range increase • FADS genes: six SNPs were genotyped (results presented for rs174556 and rs174575) • Linear regression models: • Total cholesterol, LDL, triglyceride: results presented as means ratios (log NV) • HDL: results presented as estimate βandstandarddeviation (Sd) • Adjustment: gender, study centre, age, BMI, fasting status and total dietary energy intake

  7. Study population(with genetic information)

  8. Results: Total cholesterol A: major allele / a: minor allele

  9. Results: LDL A: major allele / a: minor allele

  10. Results: Triglyceride A: major allele / a: minor allele

  11. Results: HDL A: major allele / a: minor allele

  12. Further results • No interaction between n3 PUFA and FADS genotype • No association between lipid levels and n6 PUFA intake • Similar results for the n3 PUFAs ALA, EPA, DPA and DHA • Similar results in a stratified analysis for LISA and GINI

  13. Summary • n3 PUFA: • Total cholesterol, HDL and LDL • Triglycerides • Minor allele of FADS genotype: • Total cholesterol, HDL and LDL • Triglycerides

  14. Acknowledgements • Eva Lattka • Barbara Stach • Sibylle Koletzko • Carl-Peter Bauer • Andrea von Berg • Dietrich Berdel • Ursula Krämer • BeateSchaaf • Stefan Röder • OlfHerbarth • Anette Buyken • Tim Drogies • JoachimThiery • Berthold Koletzko • Joachim Heinrich

  15. Characteristics of the FADS SNPs • Results presented for rs174556 and rs174575 • Genotype frequency a: minor allele A: major allele

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