Observational　studies　have　indicated　an　association　between　metabolic　syndrome　(MetS)　and　pruritus.　However,　the　causality　between　them　remains　unclear.　This　study　aims　to　assess　the　causality　of　MetS　and　its　components　on　pruritus.　Genetic　variation　of　MetS　and　its　components　were　selected　from　the　genome-wide　association　study　as　instrumental　variables,　with　the　inverse　variance　weighted　method　as　the　main　analytical　approach.　Univariate　and　multivariate　Mendelian　randomization　(MR)　analyses　were　used　to　assess　the　causal　effects　of　MetS　and　its　components　on　pruritus.　Sensitivity　analyses　were　performed　to　ensure　the　results＇　robustness.　Univariate　MR　analysis　indicated　no　causal　relationship　between　MetS　and　pruritus.　Among　the　components　of　MetS,　very　low-density　lipoprotein　cholesterol　(odds　ratio　[OR]　=　1.447,　95%　confidence　interval　[CI]:　1.164-1.799,　P　=　.001),　and　type　2　diabetes　(OR　=　1.131,　95%　CI:　1.009-1.266,　P　=　.034)　were　associated　with　an　increased　risk　of　pruritus.　Type　1　diabetes　was　also　positively　associated　with　pruritus　(OR　=　1.043,　95%　CI:　1.008-1.080,　P　=　.016).　Conversely,　body　mass　index　(OR　=　0.871,　95%　CI:　0.764-0.992,　P　=　.038),　obesity　(OR　=　0.705,　95%　CI:　0.543-0.915,　P　=　.009),　and　high-density　lipoprotein　cholesterol　(OR　=　0.836,　95%　CI:　0.709-0.986,　P　=　.033)　were　negatively　associated　with　the　risk　of　pruritus.　Multivariate　MR　analysis　indicated　that　the　above　relationships　remain　unchanged　after　adjusting　for　confounding　factors　(All　P　＜　.05).　This　research　demonstrates　that　MetS　as　a　whole　is　not　genetically　causal　for　pruritus,　whereas　elevated　very　low-density　lipoprotein　cholesterol　and　diabetes　significantly　heighten　the　risk　of　pruritus.　Early　identification　of　these　risk　factors　may　be　an　effective　strategy　to　reduce　the　occurrence　of　pruritus.　These　findings　challenge　the　traditional　view　that　MetS　drives　dermatological　diseases,　highlighting　that　the　contribution　of　metabolic　disturbances　to　pruritus　is　component-specific.