<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Li P</submitter><funding>National Natural Science Foundation of China</funding><funding>Natural Science Foundation of Hunan Province</funding><pagination>e3463</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10918602</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(3)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Despite numerous investigations into the relationship between physical activities (PA) and epilepsy, the causal effects remain contentious. Thus, we conducted a two-sample Mendelian randomization (MR) study to assess the potential causality.&lt;h4>Methods&lt;/h4>Single-nucleotide polymorphisms (SNPs) predisposed to self-reported moderate and vigorous physical activities (MPA and VPA) and overall acceleration average (OAA) calculated through wrist-worn accelerometers were selected as exposure instrumental variables. Five subtypes of epilepsy, including all epilepsy, focal epilepsy and generalized epilepsy (with or without each other), focal epilepsy-strict definition and generalized epilepsy-strict definition (without overlap), were chosen as the outcomes. The MR study utilized the inverse-variance weighted (IVW) method as the primary analytical tool, supplemented by MR-Egger, simple mode, weighted mode, and weighted median methods. Cochran's Q and MR-Egger intercept tests were employed to assess heterogeneity and pleiotropy, while MR pleiotropy residual sum and outlier and leave-one-out analyses were conducted to identify potential SNP outliers.&lt;h4>Results&lt;/h4>The study indicated that OAA was genetically linked to a decreased risk of both focal epilepsy (OR = 0.812, 95% CI: 0.687-0.960, p = .015, IVW) and focal epilepsy-strict definition (OR = 0.732, 95% CI: 0.596-0.900, p = .003, IVW; OR = 0.749, 95% CI: 0.573-0.979, p = .035, Weighted median). Genetically predicted MPA and VPA did not exhibit a causal association with all epilepsy or its subtypes (p>.05). No evidence of heterogeneity, pleiotropy, or SNP outlier was observed.&lt;h4>Conclusions&lt;/h4>Our findings suggested that PA with accelerometer monitoring may potentially reduce the risk of focal epilepsy, while there is no evidence supporting causal association between self-reported MPA or VPA and either focal or generalized epilepsy.</pubmed_abstract><journal>Brain and behavior</journal><pubmed_title>Genetic causal association between physical activities and epilepsy: A Mendelian randomization study.</pubmed_title><pmcid>PMC10918602</pmcid><funding_grant_id>2017JJ3500</funding_grant_id><funding_grant_id>81601139</funding_grant_id><pubmed_authors>Zhou L</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Xiao Z</pubmed_authors><pubmed_authors>Li P</pubmed_authors><pubmed_authors>Sheng D</pubmed_authors><pubmed_authors>Xiao B</pubmed_authors><pubmed_authors>Liu W</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genetic causal association between physical activities and epilepsy: A Mendelian randomization study.</name><description>&lt;h4>Background&lt;/h4>Despite numerous investigations into the relationship between physical activities (PA) and epilepsy, the causal effects remain contentious. Thus, we conducted a two-sample Mendelian randomization (MR) study to assess the potential causality.&lt;h4>Methods&lt;/h4>Single-nucleotide polymorphisms (SNPs) predisposed to self-reported moderate and vigorous physical activities (MPA and VPA) and overall acceleration average (OAA) calculated through wrist-worn accelerometers were selected as exposure instrumental variables. Five subtypes of epilepsy, including all epilepsy, focal epilepsy and generalized epilepsy (with or without each other), focal epilepsy-strict definition and generalized epilepsy-strict definition (without overlap), were chosen as the outcomes. The MR study utilized the inverse-variance weighted (IVW) method as the primary analytical tool, supplemented by MR-Egger, simple mode, weighted mode, and weighted median methods. Cochran's Q and MR-Egger intercept tests were employed to assess heterogeneity and pleiotropy, while MR pleiotropy residual sum and outlier and leave-one-out analyses were conducted to identify potential SNP outliers.&lt;h4>Results&lt;/h4>The study indicated that OAA was genetically linked to a decreased risk of both focal epilepsy (OR = 0.812, 95% CI: 0.687-0.960, p = .015, IVW) and focal epilepsy-strict definition (OR = 0.732, 95% CI: 0.596-0.900, p = .003, IVW; OR = 0.749, 95% CI: 0.573-0.979, p = .035, Weighted median). Genetically predicted MPA and VPA did not exhibit a causal association with all epilepsy or its subtypes (p>.05). No evidence of heterogeneity, pleiotropy, or SNP outlier was observed.&lt;h4>Conclusions&lt;/h4>Our findings suggested that PA with accelerometer monitoring may potentially reduce the risk of focal epilepsy, while there is no evidence supporting causal association between self-reported MPA or VPA and either focal or generalized epilepsy.</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Mar</publication><modification>2025-04-04T12:34:52.561Z</modification><creation>2025-04-04T12:34:52.561Z</creation></dates><accession>S-EPMC10918602</accession><cross_references><pubmed>38451009</pubmed><doi>10.1002/brb3.3463</doi></cross_references></HashMap>