This study aims to investigate the causal relationship between Levo-carnitine (LC) and its derivatives and schizophrenia (SZ) using a Two-sample Mendelian randomization (MR) method. Forward MR analysis was conducted using LC and its derivatives as exposure and SZ as the outcome. Candidate data were obtained from the openGWAS server. Instrumental variables (IVs) were identified as single nucleotide polymorphisms (SNPs) closely associated with exposure, and were harmonized with the outcome data after removing confounders and outliers. Hence, MR analysis was performed using inverse variance weighting (IVW) as the primary approach, and sensitivity analysis was conducted to assess the reliability and robustness of the MR results. Finally, a reverse MR analysis was carried out using the same analytical procedures as the forward one. The MR results indicate a significant negative causal relationship between isovalery-LC and SZ (P < 0.05), but in no other groups (P>0.05). Additionally, the reverse MR analysis did not identify any causal relationship between SZ and LC related exposures (P>0.05). Sensitivity analyses, including pleiotropy and heterogeneity analysis, did not reveal any potential bias on the MR results (P>0.05). The results implied that elevated levels of isovalery-LC may potentially mitigate the risk of developing SZ, thereby highlighting the prospective therapeutic and preventive implications of isovalery-LC in the clinical management of SZ.Keywords: schizophrenia; levo-carnitine; carnitine; mendelian randomization

The determination of a causal relationship between gut microbiota and a range of dyslipidemia remains uncertain. To clarify these associations, we employed a two-sample mendelian randomization (MR) analysis utilizing the inverse-variance weighted (IVW) method. This comprehensive analysis investigated the genetic variants that exhibited a significant association (p<1e-5) with 129 distinct gut microbiota genera, and their potential link to diverse forms of dyslipidemia. The results indicated a potential causal relationship between 22 gut microbiota genera and dyslipidemia in humans. Furthermore, these findings suggested that the impact of gut microbiota on dyslipidemia regulation is dependent on the specific phylum, family, and genus. Bacillota phylum demonstrated the greatest diversity, with 15 distinct genera distributed among 8 families. Notably, gut microbiota derived from the Lachnospiraceae and Lactobacillaceae families exhibit statistically significant associations with lipid levels that contribute to overall health (p<0.05). The sensitivity analysis indicated that our findings possess robustness (p>0.05). The findings of our investigation provide compelling evidence that supports a causal relationship between the gut microbiota and dyslipidemia in the human body. It is noteworthy to highlight the significant influence of the Bacillota phylum as a pivotal regulator of lipid levels, and the families Lachnospiraceae and Lactobacillaceae should be acknowledged as probiotics that make substantial contributions to this metabolic process.