Fish, Fatty Acid Biosynthesis Genes, and Multiple Sclerosis Susceptibility (S44.002)

Objective: To determine whether higher fish intake is associated with a reduced risk of multiple sclerosis (MS) and, if so, whether single nucleotide polymorphisms (SNPs) in fatty acid biosynthesis genes are also associated with MS risk.

Background: Marine diet is the best source of omega-3 polyunsaturated fatty acids (PUFAs). High fish intake has been associated with a lower risk of MS but whether this is due to PUFAs or other nutrients is unclear. SNPs in the fatty acid desaturase (FADS) gene cluster that modulate fatty acid levels have been associated with cognition, cardiovascular disease and inflammation. Whether they are associated with MS is unknown.

Design/Methods: We examined the association of fish consumption, 13 tag SNPs in FADS1, FADS2 and ELOV2 with risk of MS in 1153 individuals from the MS Sunshine Study, a multi-ethnic matched case-control study of incident MS or its precursor, clinically isolated syndrome (CIS), recruited from Kaiser Permanente Southern California. High fish intake was defined as consuming fish ≥1/week or 1–3 servings/month + fish oil supplements. Logistic regression models were utilized and adjusted for age, sex, smoking, genetic ancestry and HLADRB1*15:01.

Results: High fish intake was associated with a 45% reduced risk of MS/CIS (adjusted OR=0.55; 95%CI 0.40–0.75; p=0.0002) compared with consuming fish <1/month and no supplements. Two tag SNPs, rs174611 and rs174618, in FADS2 were independently associated with a lower risk of MS even after accounting for high fish intake (adjusted ORs 0.66, 0.64, p=0.007, 0.016, respectively).

Conclusions: These analyses support a protective role of fish consumption and PUFA biosynthesis on MS risk. These findings suggest that omega-3 fatty acids may play an important role in reducing MS risk. Future studies to replicate our findings and determine whether this is mediated by the anti-inflammatory, metabolic and/or neurological functions of PUFAs are needed.

Study Supported by: The National Institute of Neurological Disorders and Stroke (NINDS, 1R01NS075308 PI: Langer-Gould)

Disclosure: Dr. Langer-Gould has nothing to disclose. Dr. Black has nothing to disclose. Dr. Wu has nothing to disclose. Dr. Smith has nothing to disclose. Dr. Gonzales has nothing to disclose. Dr. Barcellos has nothing to disclose. Dr. Xiang has nothing to disclose. Dr. Lucas has nothing to disclose.