Can anyone translate this into 23andme results? The full study can be found under the following link. http://www.scribd.com/doc/6430904/G...elated-Genes-and-Body-Burden-of-Methylmercury BACKGROUND:Exposure to toxic methylmercury (MeHg) through ?sh consumption is a large prob- lem worldwide, and it has led to governmental recommendations of reduced ?sh consumption and blacklisting of mercury-contaminated ?sh. The elimination kinetics of MeHg varies greatly among individuals. Knowledge about the reasons for such variation is of importance for improving the risk assessment for MeHg. One possible explanation is hereditary differences in MeHg metabolism. MeHg is eliminated from the body as a glutathione (GSH) conjugate. OBJECTIVES:We conducted this study to assess the in?uence of polymorphisms in GSH-synthesizing [glutamyl-cysteine ligase modi?er subunit (GCLM-588) and glutamyl-cysteine ligase catalytic subunit (GCLC-129)] or GSH-conjugating [glutathioneS-transferase pi 1 (GSTP1-105 andGSTP1-114)] genes on MeHg retention. METHODS:Based on information obtained from questionnaires, 292 subjects from northern Sweden had a high consumption of ?sh (lean/fat ?sh two to three times per week or more). We measured total Hg in erythrocytes (Ery-Hg) and long-chain n-3 polyunsaturated fatty acids in plasma (P-PUFA; an exposure marker for ?sh intake). RESULTS:TheGSTP1 genotype modi?ed Ery-Hg; effects were seen forGSTP1-105 and -114 sepa- rately, and combining them resulted in stronger effects. We found evidence of effect modi?cation: individuals with zero or one variant allele demonstrated a steeper regression slope for Ery-Hg (p = 0.038) compared with individuals with two or more variant alleles. TheGCLM-588 genotype also in?uenced Ery-Hg (p = 0.035): Individuals with theGCLM-588 TT genotype demonstrated the highest Ery-Hg, but we saw no evidence of effect modi?cation with increasing P-PUFA. CONCLUSIONS:These results suggest a role of GSH-related polymorphisms in MeHg metabolism.