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<p>Cardiovascular disease (CVD) remains the leading cause of mortality worldwide. In addition to established risk factors such as hypertension, dyslipidemia and smoking, genetic variations may modulate individual susceptibility to CVD. The rs66698963 insertion–deletion (indel) polymorphism in the fatty‑acid desaturase (FADS) gene cluster increases fatty‑acid desaturase 1 activity and elevates circulating arachidonic acid (AA) relative to eicosapentaenoic acid (EPA). We hypothesize that carriers of the rs66698963 insertion allele develop a pro‑inflammatory AA‑dominant lipid profile that predisposes them to a greater risk of CVD. This article summarizes existing evidence linking FADS genetics, the AA/EPA ratio and inflammation and proposes observational and intervention studies to test this hypothesis. If confirmed, genotype‑based screening and targeted dietary or pharmacologic interventions could advance precision cardiovascular medicine.</p>

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Hypothesis: the rs66698963 insertion–deletion alters the AA/EPA ratio and cardiovascular disease risk

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月17日

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  • Igor Oliveira,
  • Andreas Elias Gilpin‑Falk,
  • Robert C. Block

摘要

Cardiovascular disease (CVD) remains the leading cause of mortality worldwide. In addition to established risk factors such as hypertension, dyslipidemia and smoking, genetic variations may modulate individual susceptibility to CVD. The rs66698963 insertion–deletion (indel) polymorphism in the fatty‑acid desaturase (FADS) gene cluster increases fatty‑acid desaturase 1 activity and elevates circulating arachidonic acid (AA) relative to eicosapentaenoic acid (EPA). We hypothesize that carriers of the rs66698963 insertion allele develop a pro‑inflammatory AA‑dominant lipid profile that predisposes them to a greater risk of CVD. This article summarizes existing evidence linking FADS genetics, the AA/EPA ratio and inflammation and proposes observational and intervention studies to test this hypothesis. If confirmed, genotype‑based screening and targeted dietary or pharmacologic interventions could advance precision cardiovascular medicine.