Figure 1

Study design overview for a Mendelian randomization analysis evaluating the causal effects of omega-3 polyunsaturated fatty acids on inflammatory bowel disease through circulating metabolite mediators.

Figure 2

Directed acyclic graph or causal framework illustrating the mediation Mendelian randomization approach used to assess omega-3 PUFA effects on IBD via circulating metabolites.

Figure 3

Primary Mendelian randomization results showing the estimated causal effect of omega-3 PUFA supplementation on inflammatory bowel disease risk, addressing conflicting epidemiological evidence.

Figure 4

Mediation analysis results identifying circulating metabolites that may mediate the relationship between omega-3 polyunsaturated fatty acids and inflammatory bowel disease outcomes.

Figure 5

Publication metadata for the omega-3 PUFA and IBD Mendelian randomization study, received August 2023 and published September 2023 in Metabolites.

Figure 6

Supplementary Mendelian randomization analysis (Figure 6) examining specific omega-3 fatty acid subtypes or individual metabolite pathways in relation to inflammatory bowel disease susceptibility.

Figure 7

Supplementary Mendelian randomization analysis (Figure 7) examining specific omega-3 fatty acid subtypes or individual metabolite pathways in relation to inflammatory bowel disease susceptibility.

Figure 8

Supplementary Mendelian randomization analysis (Figure 8) examining specific omega-3 fatty acid subtypes or individual metabolite pathways in relation to inflammatory bowel disease susceptibility.

Figure 9

Supplementary Mendelian randomization analysis (Figure 9) examining specific omega-3 fatty acid subtypes or individual metabolite pathways in relation to inflammatory bowel disease susceptibility.

Figure 10

Supplementary Mendelian randomization analysis (Figure 10) examining specific omega-3 fatty acid subtypes or individual metabolite pathways in relation to inflammatory bowel disease susceptibility.

Figure 11

Sensitivity analysis plot (Figure 11) from the omega-3 PUFA and IBD Mendelian randomization study, testing the robustness of causal estimates under different analytical assumptions.

Figure 12

Sensitivity analysis plot (Figure 12) from the omega-3 PUFA and IBD Mendelian randomization study, testing the robustness of causal estimates under different analytical assumptions.

Figure 13

Sensitivity analysis plot (Figure 13) from the omega-3 PUFA and IBD Mendelian randomization study, testing the robustness of causal estimates under different analytical assumptions.

Figure 14

Sensitivity analysis plot (Figure 14) from the omega-3 PUFA and IBD Mendelian randomization study, testing the robustness of causal estimates under different analytical assumptions.

Figure 15

Sensitivity analysis plot (Figure 15) from the omega-3 PUFA and IBD Mendelian randomization study, testing the robustness of causal estimates under different analytical assumptions.

Figure 16

Sensitivity analysis plot (Figure 16) from the omega-3 PUFA and IBD Mendelian randomization study, testing the robustness of causal estimates under different analytical assumptions.

Figure 17

Sensitivity analysis plot (Figure 17) from the omega-3 PUFA and IBD Mendelian randomization study, testing the robustness of causal estimates under different analytical assumptions.

Figure 18

Sensitivity analysis plot (Figure 18) from the omega-3 PUFA and IBD Mendelian randomization study, testing the robustness of causal estimates under different analytical assumptions.

Figure 19

Sensitivity analysis plot (Figure 19) from the omega-3 PUFA and IBD Mendelian randomization study, testing the robustness of causal estimates under different analytical assumptions.

Figure 20

Sensitivity analysis plot (Figure 20) from the omega-3 PUFA and IBD Mendelian randomization study, testing the robustness of causal estimates under different analytical assumptions.

Figure 21

Forest plot or scatter plot (Figure 21) presenting individual SNP-level estimates for the association between genetically predicted omega-3 PUFA levels and inflammatory bowel disease risk.

Figure 22

Forest plot or scatter plot (Figure 22) presenting individual SNP-level estimates for the association between genetically predicted omega-3 PUFA levels and inflammatory bowel disease risk.

Figure 23

Forest plot or scatter plot (Figure 23) presenting individual SNP-level estimates for the association between genetically predicted omega-3 PUFA levels and inflammatory bowel disease risk.

Figure 24

Forest plot or scatter plot (Figure 24) presenting individual SNP-level estimates for the association between genetically predicted omega-3 PUFA levels and inflammatory bowel disease risk.

Figure 25

Forest plot or scatter plot (Figure 25) presenting individual SNP-level estimates for the association between genetically predicted omega-3 PUFA levels and inflammatory bowel disease risk.

Figure 26

Forest plot or scatter plot (Figure 26) presenting individual SNP-level estimates for the association between genetically predicted omega-3 PUFA levels and inflammatory bowel disease risk.

Figure 27

Forest plot or scatter plot (Figure 27) presenting individual SNP-level estimates for the association between genetically predicted omega-3 PUFA levels and inflammatory bowel disease risk.

Figure 28

Forest plot or scatter plot (Figure 28) presenting individual SNP-level estimates for the association between genetically predicted omega-3 PUFA levels and inflammatory bowel disease risk.

Figure 29

Forest plot or scatter plot (Figure 29) presenting individual SNP-level estimates for the association between genetically predicted omega-3 PUFA levels and inflammatory bowel disease risk.

Figure 30

Forest plot or scatter plot (Figure 30) presenting individual SNP-level estimates for the association between genetically predicted omega-3 PUFA levels and inflammatory bowel disease risk.

Figure 31

Forest plot or scatter plot (Figure 31) presenting individual SNP-level estimates for the association between genetically predicted omega-3 PUFA levels and inflammatory bowel disease risk.

Figure 32

Forest plot or scatter plot (Figure 32) presenting individual SNP-level estimates for the association between genetically predicted omega-3 PUFA levels and inflammatory bowel disease risk.

Figure 33

Forest plot or scatter plot (Figure 33) presenting individual SNP-level estimates for the association between genetically predicted omega-3 PUFA levels and inflammatory bowel disease risk.

Figure 34

Forest plot or scatter plot (Figure 34) presenting individual SNP-level estimates for the association between genetically predicted omega-3 PUFA levels and inflammatory bowel disease risk.

Figure 35

Forest plot or scatter plot (Figure 35) presenting individual SNP-level estimates for the association between genetically predicted omega-3 PUFA levels and inflammatory bowel disease risk.

Figure 36

Leave-one-out or funnel plot analysis (Figure 36) assessing potential pleiotropy and outlier influence in the omega-3 PUFA and IBD Mendelian randomization framework.

Figure 37

Leave-one-out or funnel plot analysis (Figure 37) assessing potential pleiotropy and outlier influence in the omega-3 PUFA and IBD Mendelian randomization framework.

Figure 38

Leave-one-out or funnel plot analysis (Figure 38) assessing potential pleiotropy and outlier influence in the omega-3 PUFA and IBD Mendelian randomization framework.

Figure 39

Leave-one-out or funnel plot analysis (Figure 39) assessing potential pleiotropy and outlier influence in the omega-3 PUFA and IBD Mendelian randomization framework.

Figure 40

Leave-one-out or funnel plot analysis (Figure 40) assessing potential pleiotropy and outlier influence in the omega-3 PUFA and IBD Mendelian randomization framework.

Figure 41

Leave-one-out or funnel plot analysis (Figure 41) assessing potential pleiotropy and outlier influence in the omega-3 PUFA and IBD Mendelian randomization framework.

Figure 42

Leave-one-out or funnel plot analysis (Figure 42) assessing potential pleiotropy and outlier influence in the omega-3 PUFA and IBD Mendelian randomization framework.

Figure 43

Leave-one-out or funnel plot analysis (Figure 43) assessing potential pleiotropy and outlier influence in the omega-3 PUFA and IBD Mendelian randomization framework.

Figure 44

Leave-one-out or funnel plot analysis (Figure 44) assessing potential pleiotropy and outlier influence in the omega-3 PUFA and IBD Mendelian randomization framework.

Figure 45

Leave-one-out or funnel plot analysis (Figure 45) assessing potential pleiotropy and outlier influence in the omega-3 PUFA and IBD Mendelian randomization framework.

Figure 46

Leave-one-out or funnel plot analysis (Figure 46) assessing potential pleiotropy and outlier influence in the omega-3 PUFA and IBD Mendelian randomization framework.

Figure 47

Leave-one-out or funnel plot analysis (Figure 47) assessing potential pleiotropy and outlier influence in the omega-3 PUFA and IBD Mendelian randomization framework.

Figure 48

Leave-one-out or funnel plot analysis (Figure 48) assessing potential pleiotropy and outlier influence in the omega-3 PUFA and IBD Mendelian randomization framework.

Figure 49

Leave-one-out or funnel plot analysis (Figure 49) assessing potential pleiotropy and outlier influence in the omega-3 PUFA and IBD Mendelian randomization framework.

Figure 50

Leave-one-out or funnel plot analysis (Figure 50) assessing potential pleiotropy and outlier influence in the omega-3 PUFA and IBD Mendelian randomization framework.

Figure 51

Metabolite-specific mediation result (Figure 51) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 52

Metabolite-specific mediation result (Figure 52) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 53

Metabolite-specific mediation result (Figure 53) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 54

Metabolite-specific mediation result (Figure 54) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 55

Metabolite-specific mediation result (Figure 55) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 56

Metabolite-specific mediation result (Figure 56) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 57

Metabolite-specific mediation result (Figure 57) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 58

Metabolite-specific mediation result (Figure 58) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 59

Metabolite-specific mediation result (Figure 59) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 60

Metabolite-specific mediation result (Figure 60) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 61

Metabolite-specific mediation result (Figure 61) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 62

Metabolite-specific mediation result (Figure 62) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 63

Metabolite-specific mediation result (Figure 63) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 64

Metabolite-specific mediation result (Figure 64) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 65

Metabolite-specific mediation result (Figure 65) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 66

Metabolite-specific mediation result (Figure 66) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 67

Metabolite-specific mediation result (Figure 67) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 68

Metabolite-specific mediation result (Figure 68) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 69

Metabolite-specific mediation result (Figure 69) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 70

Metabolite-specific mediation result (Figure 70) quantifying the proportion of the omega-3 PUFA effect on IBD that operates through a particular circulating metabolite pathway.

Figure 71

Subgroup or stratified analysis (Figure 71) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 72

Subgroup or stratified analysis (Figure 72) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 73

Subgroup or stratified analysis (Figure 73) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 74

Subgroup or stratified analysis (Figure 74) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 75

Subgroup or stratified analysis (Figure 75) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 76

Subgroup or stratified analysis (Figure 76) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 77

Subgroup or stratified analysis (Figure 77) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 78

Subgroup or stratified analysis (Figure 78) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 79

Subgroup or stratified analysis (Figure 79) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 80

Subgroup or stratified analysis (Figure 80) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 81

Subgroup or stratified analysis (Figure 81) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 82

Subgroup or stratified analysis (Figure 82) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 83

Subgroup or stratified analysis (Figure 83) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 84

Subgroup or stratified analysis (Figure 84) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 85

Subgroup or stratified analysis (Figure 85) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 86

Subgroup or stratified analysis (Figure 86) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 87

Subgroup or stratified analysis (Figure 87) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 88

Subgroup or stratified analysis (Figure 88) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 89

Subgroup or stratified analysis (Figure 89) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 90

Subgroup or stratified analysis (Figure 90) from the Mendelian randomization study, examining omega-3 PUFA effects separately for Crohn's disease and ulcerative colitis.

Figure 91

Supplementary statistical plot (Figure 91) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 92

Supplementary statistical plot (Figure 92) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 93

Supplementary statistical plot (Figure 93) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 94

Supplementary statistical plot (Figure 94) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 95

Supplementary statistical plot (Figure 95) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 96

Supplementary statistical plot (Figure 96) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 97

Supplementary statistical plot (Figure 97) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 98

Supplementary statistical plot (Figure 98) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 99

Supplementary statistical plot (Figure 99) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 100

Supplementary statistical plot (Figure 100) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 101

Supplementary statistical plot (Figure 101) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 102

Supplementary statistical plot (Figure 102) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 103

Supplementary statistical plot (Figure 103) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 104

Supplementary statistical plot (Figure 104) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 105

Supplementary statistical plot (Figure 105) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 106

Supplementary statistical plot (Figure 106) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 107

Supplementary statistical plot (Figure 107) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 108

Supplementary statistical plot (Figure 108) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 109

Supplementary statistical plot (Figure 109) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 110

Supplementary statistical plot (Figure 110) providing additional evidence on the causal pathway between omega-3 polyunsaturated fatty acids and inflammatory bowel disease through circulating metabolites.

Figure 111

Extended analysis figure (Figure 111) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 112

Extended analysis figure (Figure 112) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 113

Extended analysis figure (Figure 113) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 114

Extended analysis figure (Figure 114) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 115

Extended analysis figure (Figure 115) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 116

Extended analysis figure (Figure 116) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 117

Extended analysis figure (Figure 117) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 118

Extended analysis figure (Figure 118) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 119

Extended analysis figure (Figure 119) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 120

Extended analysis figure (Figure 120) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 121

Extended analysis figure (Figure 121) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 122

Extended analysis figure (Figure 122) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 123

Extended analysis figure (Figure 123) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 124

Extended analysis figure (Figure 124) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 125

Extended analysis figure (Figure 125) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 126

Extended analysis figure (Figure 126) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 127

Extended analysis figure (Figure 127) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 128

Extended analysis figure (Figure 128) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 129

Extended analysis figure (Figure 129) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 130

Extended analysis figure (Figure 130) from the omega-3 PUFA and IBD study, presenting results for additional metabolite mediators or alternative instrument variable selections.

Figure 131

Robustness check (Figure 131) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 132

Robustness check (Figure 132) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 133

Robustness check (Figure 133) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 134

Robustness check (Figure 134) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 135

Robustness check (Figure 135) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 136

Robustness check (Figure 136) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 137

Robustness check (Figure 137) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 138

Robustness check (Figure 138) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 139

Robustness check (Figure 139) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 140

Robustness check (Figure 140) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 141

Robustness check (Figure 141) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 142

Robustness check (Figure 142) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 143

Robustness check (Figure 143) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 144

Robustness check (Figure 144) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 145

Robustness check (Figure 145) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 146

Robustness check (Figure 146) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 147

Robustness check (Figure 147) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 148

Robustness check (Figure 148) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 149

Robustness check (Figure 149) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 150

Robustness check (Figure 150) from the mediation Mendelian randomization analysis, validating the omega-3 PUFA and IBD causal pathway using weighted median or MR-Egger methods.

Figure 151

Metabolomic pathway visualization (Figure 151) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 152

Metabolomic pathway visualization (Figure 152) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 153

Metabolomic pathway visualization (Figure 153) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 154

Metabolomic pathway visualization (Figure 154) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 155

Metabolomic pathway visualization (Figure 155) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 156

Metabolomic pathway visualization (Figure 156) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 157

Metabolomic pathway visualization (Figure 157) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 158

Metabolomic pathway visualization (Figure 158) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 159

Metabolomic pathway visualization (Figure 159) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 160

Metabolomic pathway visualization (Figure 160) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 161

Metabolomic pathway visualization (Figure 161) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 162

Metabolomic pathway visualization (Figure 162) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 163

Metabolomic pathway visualization (Figure 163) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 164

Metabolomic pathway visualization (Figure 164) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 165

Metabolomic pathway visualization (Figure 165) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 166

Metabolomic pathway visualization (Figure 166) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 167

Metabolomic pathway visualization (Figure 167) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 168

Metabolomic pathway visualization (Figure 168) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 169

Metabolomic pathway visualization (Figure 169) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 170

Metabolomic pathway visualization (Figure 170) mapping the intermediary role of specific circulating metabolites in the omega-3 PUFA and inflammatory bowel disease relationship.

Figure 171

Additional MR analysis (Figure 171) exploring dose-response relationships or nonlinear effects of omega-3 PUFA levels on IBD risk.

Figure 172

Additional MR analysis (Figure 172) exploring dose-response relationships or nonlinear effects of omega-3 PUFA levels on IBD risk.

Figure 173

Additional MR analysis (Figure 173) exploring dose-response relationships or nonlinear effects of omega-3 PUFA levels on IBD risk.

Figure 174

Additional MR analysis (Figure 174) exploring dose-response relationships or nonlinear effects of omega-3 PUFA levels on IBD risk.

Figure 175

Additional MR analysis (Figure 175) exploring dose-response relationships or nonlinear effects of omega-3 PUFA levels on IBD risk.

Figure 176

Additional MR analysis (Figure 176) exploring dose-response relationships or nonlinear effects of omega-3 PUFA levels on IBD risk.

Figure 177

Additional MR analysis (Figure 177) exploring dose-response relationships or nonlinear effects of omega-3 PUFA levels on IBD risk.

Figure 178

Additional MR analysis (Figure 178) exploring dose-response relationships or nonlinear effects of omega-3 PUFA levels on IBD risk.

Figure 179

Additional MR analysis (Figure 179) exploring dose-response relationships or nonlinear effects of omega-3 PUFA levels on IBD risk.

Figure 180

Additional MR analysis (Figure 180) exploring dose-response relationships or nonlinear effects of omega-3 PUFA levels on IBD risk.

Figure 181

Additional MR analysis (Figure 181) exploring dose-response relationships or nonlinear effects of omega-3 PUFA levels on IBD risk.

Figure 182

Additional MR analysis (Figure 182) exploring dose-response relationships or nonlinear effects of omega-3 PUFA levels on IBD risk.

Figure 183

Additional MR analysis (Figure 183) exploring dose-response relationships or nonlinear effects of omega-3 PUFA levels on IBD risk.

Figure 184

Additional MR analysis (Figure 184) exploring dose-response relationships or nonlinear effects of omega-3 PUFA levels on IBD risk.

Figure 185

Regional association plot (Figure 185) showing genetic loci associated with omega-3 fatty acid levels, including alpha-linolenic, eicosapentaenoic, and docosahexaenoic acids in relation to Crohn's disease and ulcerative colitis.

Figure 186

Supplementary figure (Figure 186) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 187

Supplementary figure (Figure 187) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 188

Supplementary figure (Figure 188) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 189

Supplementary figure (Figure 189) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 190

Supplementary figure (Figure 190) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 191

Supplementary figure (Figure 191) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 192

Supplementary figure (Figure 192) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 193

Supplementary figure (Figure 193) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 194

Supplementary figure (Figure 194) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 195

Supplementary figure (Figure 195) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 196

Supplementary figure (Figure 196) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 197

Supplementary figure (Figure 197) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 198

Supplementary figure (Figure 198) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 199

Supplementary figure (Figure 199) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 200

Supplementary figure (Figure 200) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 201

Supplementary figure (Figure 201) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 202

Supplementary figure (Figure 202) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 203

Supplementary figure (Figure 203) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 204

Supplementary figure (Figure 204) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 205

Supplementary figure (Figure 205) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 206

Supplementary figure (Figure 206) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 207

Supplementary figure (Figure 207) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 208

Supplementary figure (Figure 208) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 209

Supplementary figure (Figure 209) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 210

Supplementary figure (Figure 210) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 211

Supplementary figure (Figure 211) from a comprehensive Mendelian randomization study with over 200 analyses examining omega-3 polyunsaturated fatty acid effects on inflammatory bowel disease via circulating metabolite mediators.

Figure 212

Scatter plot depicting the causal effect estimates of individual genetic instruments for total omega-3 fatty acids on inflammatory bowel disease (IBD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 213

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of total omega-3 fatty acids on inflammatory bowel disease (IBD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 214

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of total omega-3 fatty acids and inflammatory bowel disease (IBD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 215

Leave-one-out sensitivity analysis for the causal relationship between total omega-3 fatty acids and inflammatory bowel disease (IBD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 216

Mediation analysis diagram illustrating the potential pathway through which total omega-3 fatty acids may influence inflammatory bowel disease (IBD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 217

Scatter plot depicting the causal effect estimates of individual genetic instruments for total omega-3 fatty acids on inflammatory bowel disease (IBD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 218

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of total omega-3 fatty acids on inflammatory bowel disease (IBD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 219

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of total omega-3 fatty acids and inflammatory bowel disease (IBD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 220

Leave-one-out sensitivity analysis for the causal relationship between total omega-3 fatty acids and inflammatory bowel disease (IBD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 221

Mediation analysis diagram illustrating the potential pathway through which total omega-3 fatty acids may influence inflammatory bowel disease (IBD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 222

Scatter plot depicting the causal effect estimates of individual genetic instruments for total omega-3 fatty acids on inflammatory bowel disease (IBD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 223

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of total omega-3 fatty acids on inflammatory bowel disease (IBD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 224

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of total omega-3 fatty acids and inflammatory bowel disease (IBD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 225

Leave-one-out sensitivity analysis for the causal relationship between total omega-3 fatty acids and inflammatory bowel disease (IBD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 226

Mediation analysis diagram illustrating the potential pathway through which total omega-3 fatty acids may influence inflammatory bowel disease (IBD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 227

Scatter plot depicting the causal effect estimates of individual genetic instruments for total omega-3 fatty acids on inflammatory bowel disease (IBD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 228

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of total omega-3 fatty acids on inflammatory bowel disease (IBD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 229

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of total omega-3 fatty acids and inflammatory bowel disease (IBD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 230

Leave-one-out sensitivity analysis for the causal relationship between total omega-3 fatty acids and inflammatory bowel disease (IBD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 231

Mediation analysis diagram illustrating the potential pathway through which total omega-3 fatty acids may influence inflammatory bowel disease (IBD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 232

Scatter plot depicting the causal effect estimates of individual genetic instruments for total omega-3 fatty acids on Crohn's disease (CD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 233

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of total omega-3 fatty acids on Crohn's disease (CD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 234

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of total omega-3 fatty acids and Crohn's disease (CD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 235

Leave-one-out sensitivity analysis for the causal relationship between total omega-3 fatty acids and Crohn's disease (CD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 236

Mediation analysis diagram illustrating the potential pathway through which total omega-3 fatty acids may influence Crohn's disease (CD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 237

Scatter plot depicting the causal effect estimates of individual genetic instruments for total omega-3 fatty acids on Crohn's disease (CD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 238

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of total omega-3 fatty acids on Crohn's disease (CD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 239

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of total omega-3 fatty acids and Crohn's disease (CD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 240

Leave-one-out sensitivity analysis for the causal relationship between total omega-3 fatty acids and Crohn's disease (CD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 241

Mediation analysis diagram illustrating the potential pathway through which total omega-3 fatty acids may influence Crohn's disease (CD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 242

Scatter plot depicting the causal effect estimates of individual genetic instruments for total omega-3 fatty acids on Crohn's disease (CD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 243

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of total omega-3 fatty acids on Crohn's disease (CD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 244

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of total omega-3 fatty acids and Crohn's disease (CD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 245

Leave-one-out sensitivity analysis for the causal relationship between total omega-3 fatty acids and Crohn's disease (CD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 246

Mediation analysis diagram illustrating the potential pathway through which total omega-3 fatty acids may influence Crohn's disease (CD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 247

Scatter plot depicting the causal effect estimates of individual genetic instruments for total omega-3 fatty acids on Crohn's disease (CD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 248

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of total omega-3 fatty acids on Crohn's disease (CD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 249

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of total omega-3 fatty acids and Crohn's disease (CD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 250

Leave-one-out sensitivity analysis for the causal relationship between total omega-3 fatty acids and Crohn's disease (CD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 251

Mediation analysis diagram illustrating the potential pathway through which total omega-3 fatty acids may influence Crohn's disease (CD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 252

Scatter plot depicting the causal effect estimates of individual genetic instruments for total omega-3 fatty acids on ulcerative colitis (UC), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 253

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of total omega-3 fatty acids on ulcerative colitis (UC). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 254

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of total omega-3 fatty acids and ulcerative colitis (UC). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 255

Leave-one-out sensitivity analysis for the causal relationship between total omega-3 fatty acids and ulcerative colitis (UC). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 256

Mediation analysis diagram illustrating the potential pathway through which total omega-3 fatty acids may influence ulcerative colitis (UC) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 257

Scatter plot depicting the causal effect estimates of individual genetic instruments for total omega-3 fatty acids on ulcerative colitis (UC), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 258

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of total omega-3 fatty acids on ulcerative colitis (UC). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 259

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of total omega-3 fatty acids and ulcerative colitis (UC). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 260

Leave-one-out sensitivity analysis for the causal relationship between total omega-3 fatty acids and ulcerative colitis (UC). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 261

Mediation analysis diagram illustrating the potential pathway through which total omega-3 fatty acids may influence ulcerative colitis (UC) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 262

Scatter plot depicting the causal effect estimates of individual genetic instruments for total omega-3 fatty acids on ulcerative colitis (UC), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 263

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of total omega-3 fatty acids on ulcerative colitis (UC). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 264

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of total omega-3 fatty acids and ulcerative colitis (UC). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 265

Leave-one-out sensitivity analysis for the causal relationship between total omega-3 fatty acids and ulcerative colitis (UC). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 266

Mediation analysis diagram illustrating the potential pathway through which total omega-3 fatty acids may influence ulcerative colitis (UC) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 267

Scatter plot depicting the causal effect estimates of individual genetic instruments for total omega-3 fatty acids on ulcerative colitis (UC), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 268

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of total omega-3 fatty acids on ulcerative colitis (UC). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 269

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of total omega-3 fatty acids and ulcerative colitis (UC). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 270

Leave-one-out sensitivity analysis for the causal relationship between total omega-3 fatty acids and ulcerative colitis (UC). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 271

Mediation analysis diagram illustrating the potential pathway through which total omega-3 fatty acids may influence ulcerative colitis (UC) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 272

Scatter plot depicting the causal effect estimates of individual genetic instruments for alpha-linolenic acid (ALA) on inflammatory bowel disease (IBD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 273

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of alpha-linolenic acid (ALA) on inflammatory bowel disease (IBD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 274

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of alpha-linolenic acid (ALA) and inflammatory bowel disease (IBD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 275

Leave-one-out sensitivity analysis for the causal relationship between alpha-linolenic acid (ALA) and inflammatory bowel disease (IBD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 276

Mediation analysis diagram illustrating the potential pathway through which alpha-linolenic acid (ALA) may influence inflammatory bowel disease (IBD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 277

Scatter plot depicting the causal effect estimates of individual genetic instruments for alpha-linolenic acid (ALA) on inflammatory bowel disease (IBD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 278

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of alpha-linolenic acid (ALA) on inflammatory bowel disease (IBD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 279

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of alpha-linolenic acid (ALA) and inflammatory bowel disease (IBD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 280

Leave-one-out sensitivity analysis for the causal relationship between alpha-linolenic acid (ALA) and inflammatory bowel disease (IBD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 281

Mediation analysis diagram illustrating the potential pathway through which alpha-linolenic acid (ALA) may influence inflammatory bowel disease (IBD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 282

Scatter plot depicting the causal effect estimates of individual genetic instruments for alpha-linolenic acid (ALA) on inflammatory bowel disease (IBD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 283

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of alpha-linolenic acid (ALA) on inflammatory bowel disease (IBD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 284

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of alpha-linolenic acid (ALA) and inflammatory bowel disease (IBD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 285

Leave-one-out sensitivity analysis for the causal relationship between alpha-linolenic acid (ALA) and inflammatory bowel disease (IBD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 286

Mediation analysis diagram illustrating the potential pathway through which alpha-linolenic acid (ALA) may influence inflammatory bowel disease (IBD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 287

Scatter plot depicting the causal effect estimates of individual genetic instruments for alpha-linolenic acid (ALA) on inflammatory bowel disease (IBD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 288

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of alpha-linolenic acid (ALA) on inflammatory bowel disease (IBD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 289

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of alpha-linolenic acid (ALA) and inflammatory bowel disease (IBD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 290

Leave-one-out sensitivity analysis for the causal relationship between alpha-linolenic acid (ALA) and inflammatory bowel disease (IBD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 291

Mediation analysis diagram illustrating the potential pathway through which alpha-linolenic acid (ALA) may influence inflammatory bowel disease (IBD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 292

Scatter plot depicting the causal effect estimates of individual genetic instruments for alpha-linolenic acid (ALA) on Crohn's disease (CD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 293

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of alpha-linolenic acid (ALA) on Crohn's disease (CD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 294

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of alpha-linolenic acid (ALA) and Crohn's disease (CD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 295

Leave-one-out sensitivity analysis for the causal relationship between alpha-linolenic acid (ALA) and Crohn's disease (CD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 296

Mediation analysis diagram illustrating the potential pathway through which alpha-linolenic acid (ALA) may influence Crohn's disease (CD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 297

Scatter plot depicting the causal effect estimates of individual genetic instruments for alpha-linolenic acid (ALA) on Crohn's disease (CD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 298

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of alpha-linolenic acid (ALA) on Crohn's disease (CD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 299

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of alpha-linolenic acid (ALA) and Crohn's disease (CD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 300

Leave-one-out sensitivity analysis for the causal relationship between alpha-linolenic acid (ALA) and Crohn's disease (CD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 301

Mediation analysis diagram illustrating the potential pathway through which alpha-linolenic acid (ALA) may influence Crohn's disease (CD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 302

Scatter plot depicting the causal effect estimates of individual genetic instruments for alpha-linolenic acid (ALA) on Crohn's disease (CD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 303

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of alpha-linolenic acid (ALA) on Crohn's disease (CD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 304

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of alpha-linolenic acid (ALA) and Crohn's disease (CD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 305

Leave-one-out sensitivity analysis for the causal relationship between alpha-linolenic acid (ALA) and Crohn's disease (CD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 306

Mediation analysis diagram illustrating the potential pathway through which alpha-linolenic acid (ALA) may influence Crohn's disease (CD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 307

Scatter plot depicting the causal effect estimates of individual genetic instruments for alpha-linolenic acid (ALA) on Crohn's disease (CD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 308

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of alpha-linolenic acid (ALA) on Crohn's disease (CD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 309

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of alpha-linolenic acid (ALA) and Crohn's disease (CD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 310

Leave-one-out sensitivity analysis for the causal relationship between alpha-linolenic acid (ALA) and Crohn's disease (CD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 311

Mediation analysis diagram illustrating the potential pathway through which alpha-linolenic acid (ALA) may influence Crohn's disease (CD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 312

Scatter plot depicting the causal effect estimates of individual genetic instruments for alpha-linolenic acid (ALA) on ulcerative colitis (UC), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 313

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of alpha-linolenic acid (ALA) on ulcerative colitis (UC). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 314

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of alpha-linolenic acid (ALA) and ulcerative colitis (UC). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 315

Leave-one-out sensitivity analysis for the causal relationship between alpha-linolenic acid (ALA) and ulcerative colitis (UC). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 316

Mediation analysis diagram illustrating the potential pathway through which alpha-linolenic acid (ALA) may influence ulcerative colitis (UC) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 317

Scatter plot depicting the causal effect estimates of individual genetic instruments for alpha-linolenic acid (ALA) on ulcerative colitis (UC), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 318

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of alpha-linolenic acid (ALA) on ulcerative colitis (UC). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 319

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of alpha-linolenic acid (ALA) and ulcerative colitis (UC). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 320

Leave-one-out sensitivity analysis for the causal relationship between alpha-linolenic acid (ALA) and ulcerative colitis (UC). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 321

Mediation analysis diagram illustrating the potential pathway through which alpha-linolenic acid (ALA) may influence ulcerative colitis (UC) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 322

Scatter plot depicting the causal effect estimates of individual genetic instruments for alpha-linolenic acid (ALA) on ulcerative colitis (UC), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 323

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of alpha-linolenic acid (ALA) on ulcerative colitis (UC). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 324

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of alpha-linolenic acid (ALA) and ulcerative colitis (UC). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 325

Leave-one-out sensitivity analysis for the causal relationship between alpha-linolenic acid (ALA) and ulcerative colitis (UC). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 326

Mediation analysis diagram illustrating the potential pathway through which alpha-linolenic acid (ALA) may influence ulcerative colitis (UC) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 327

Scatter plot depicting the causal effect estimates of individual genetic instruments for alpha-linolenic acid (ALA) on ulcerative colitis (UC), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 328

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of alpha-linolenic acid (ALA) on ulcerative colitis (UC). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 329

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of alpha-linolenic acid (ALA) and ulcerative colitis (UC). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 330

Leave-one-out sensitivity analysis for the causal relationship between alpha-linolenic acid (ALA) and ulcerative colitis (UC). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 331

Mediation analysis diagram illustrating the potential pathway through which alpha-linolenic acid (ALA) may influence ulcerative colitis (UC) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 332

Scatter plot depicting the causal effect estimates of individual genetic instruments for eicosapentaenoic acid (EPA) on inflammatory bowel disease (IBD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 333

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of eicosapentaenoic acid (EPA) on inflammatory bowel disease (IBD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 334

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of eicosapentaenoic acid (EPA) and inflammatory bowel disease (IBD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 335

Leave-one-out sensitivity analysis for the causal relationship between eicosapentaenoic acid (EPA) and inflammatory bowel disease (IBD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 336

Mediation analysis diagram illustrating the potential pathway through which eicosapentaenoic acid (EPA) may influence inflammatory bowel disease (IBD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 337

Scatter plot depicting the causal effect estimates of individual genetic instruments for eicosapentaenoic acid (EPA) on inflammatory bowel disease (IBD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 338

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of eicosapentaenoic acid (EPA) on inflammatory bowel disease (IBD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 339

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of eicosapentaenoic acid (EPA) and inflammatory bowel disease (IBD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 340

Leave-one-out sensitivity analysis for the causal relationship between eicosapentaenoic acid (EPA) and inflammatory bowel disease (IBD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 341

Mediation analysis diagram illustrating the potential pathway through which eicosapentaenoic acid (EPA) may influence inflammatory bowel disease (IBD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 342

Scatter plot depicting the causal effect estimates of individual genetic instruments for eicosapentaenoic acid (EPA) on inflammatory bowel disease (IBD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 343

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of eicosapentaenoic acid (EPA) on inflammatory bowel disease (IBD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 344

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of eicosapentaenoic acid (EPA) and inflammatory bowel disease (IBD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 345

Leave-one-out sensitivity analysis for the causal relationship between eicosapentaenoic acid (EPA) and inflammatory bowel disease (IBD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 346

Mediation analysis diagram illustrating the potential pathway through which eicosapentaenoic acid (EPA) may influence inflammatory bowel disease (IBD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 347

Scatter plot depicting the causal effect estimates of individual genetic instruments for eicosapentaenoic acid (EPA) on inflammatory bowel disease (IBD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 348

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of eicosapentaenoic acid (EPA) on inflammatory bowel disease (IBD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 349

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of eicosapentaenoic acid (EPA) and inflammatory bowel disease (IBD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 350

Leave-one-out sensitivity analysis for the causal relationship between eicosapentaenoic acid (EPA) and inflammatory bowel disease (IBD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 351

Mediation analysis diagram illustrating the potential pathway through which eicosapentaenoic acid (EPA) may influence inflammatory bowel disease (IBD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 352

Scatter plot depicting the causal effect estimates of individual genetic instruments for eicosapentaenoic acid (EPA) on Crohn's disease (CD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 353

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of eicosapentaenoic acid (EPA) on Crohn's disease (CD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 354

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of eicosapentaenoic acid (EPA) and Crohn's disease (CD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 355

Leave-one-out sensitivity analysis for the causal relationship between eicosapentaenoic acid (EPA) and Crohn's disease (CD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 356

Mediation analysis diagram illustrating the potential pathway through which eicosapentaenoic acid (EPA) may influence Crohn's disease (CD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 357

Scatter plot depicting the causal effect estimates of individual genetic instruments for eicosapentaenoic acid (EPA) on Crohn's disease (CD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 358

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of eicosapentaenoic acid (EPA) on Crohn's disease (CD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 359

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of eicosapentaenoic acid (EPA) and Crohn's disease (CD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 360

Leave-one-out sensitivity analysis for the causal relationship between eicosapentaenoic acid (EPA) and Crohn's disease (CD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 361

Mediation analysis diagram illustrating the potential pathway through which eicosapentaenoic acid (EPA) may influence Crohn's disease (CD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 362

Scatter plot depicting the causal effect estimates of individual genetic instruments for eicosapentaenoic acid (EPA) on Crohn's disease (CD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 363

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of eicosapentaenoic acid (EPA) on Crohn's disease (CD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 364

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of eicosapentaenoic acid (EPA) and Crohn's disease (CD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 365

Leave-one-out sensitivity analysis for the causal relationship between eicosapentaenoic acid (EPA) and Crohn's disease (CD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 366

Mediation analysis diagram illustrating the potential pathway through which eicosapentaenoic acid (EPA) may influence Crohn's disease (CD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 367

Scatter plot depicting the causal effect estimates of individual genetic instruments for eicosapentaenoic acid (EPA) on Crohn's disease (CD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 368

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of eicosapentaenoic acid (EPA) on Crohn's disease (CD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 369

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of eicosapentaenoic acid (EPA) and Crohn's disease (CD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 370

Leave-one-out sensitivity analysis for the causal relationship between eicosapentaenoic acid (EPA) and Crohn's disease (CD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 371

Mediation analysis diagram illustrating the potential pathway through which eicosapentaenoic acid (EPA) may influence Crohn's disease (CD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 372

Scatter plot depicting the causal effect estimates of individual genetic instruments for eicosapentaenoic acid (EPA) on ulcerative colitis (UC), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 373

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of eicosapentaenoic acid (EPA) on ulcerative colitis (UC). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 374

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of eicosapentaenoic acid (EPA) and ulcerative colitis (UC). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 375

Leave-one-out sensitivity analysis for the causal relationship between eicosapentaenoic acid (EPA) and ulcerative colitis (UC). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 376

Mediation analysis diagram illustrating the potential pathway through which eicosapentaenoic acid (EPA) may influence ulcerative colitis (UC) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 377

Scatter plot depicting the causal effect estimates of individual genetic instruments for eicosapentaenoic acid (EPA) on ulcerative colitis (UC), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 378

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of eicosapentaenoic acid (EPA) on ulcerative colitis (UC). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 379

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of eicosapentaenoic acid (EPA) and ulcerative colitis (UC). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 380

Leave-one-out sensitivity analysis for the causal relationship between eicosapentaenoic acid (EPA) and ulcerative colitis (UC). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 381

Mediation analysis diagram illustrating the potential pathway through which eicosapentaenoic acid (EPA) may influence ulcerative colitis (UC) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 382

Scatter plot depicting the causal effect estimates of individual genetic instruments for eicosapentaenoic acid (EPA) on ulcerative colitis (UC), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 383

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of eicosapentaenoic acid (EPA) on ulcerative colitis (UC). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 384

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of eicosapentaenoic acid (EPA) and ulcerative colitis (UC). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 385

Leave-one-out sensitivity analysis for the causal relationship between eicosapentaenoic acid (EPA) and ulcerative colitis (UC). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 386

Mediation analysis diagram illustrating the potential pathway through which eicosapentaenoic acid (EPA) may influence ulcerative colitis (UC) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 387

Scatter plot depicting the causal effect estimates of individual genetic instruments for eicosapentaenoic acid (EPA) on ulcerative colitis (UC), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 388

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of eicosapentaenoic acid (EPA) on ulcerative colitis (UC). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 389

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of eicosapentaenoic acid (EPA) and ulcerative colitis (UC). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 390

Leave-one-out sensitivity analysis for the causal relationship between eicosapentaenoic acid (EPA) and ulcerative colitis (UC). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 391

Mediation analysis diagram illustrating the potential pathway through which eicosapentaenoic acid (EPA) may influence ulcerative colitis (UC) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 392

Scatter plot depicting the causal effect estimates of individual genetic instruments for docosahexaenoic acid (DHA) on inflammatory bowel disease (IBD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 393

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of docosahexaenoic acid (DHA) on inflammatory bowel disease (IBD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 394

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of docosahexaenoic acid (DHA) and inflammatory bowel disease (IBD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 395

Leave-one-out sensitivity analysis for the causal relationship between docosahexaenoic acid (DHA) and inflammatory bowel disease (IBD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 396

Mediation analysis diagram illustrating the potential pathway through which docosahexaenoic acid (DHA) may influence inflammatory bowel disease (IBD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 397

Scatter plot depicting the causal effect estimates of individual genetic instruments for docosahexaenoic acid (DHA) on inflammatory bowel disease (IBD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 398

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of docosahexaenoic acid (DHA) on inflammatory bowel disease (IBD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 399

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of docosahexaenoic acid (DHA) and inflammatory bowel disease (IBD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 400

Leave-one-out sensitivity analysis for the causal relationship between docosahexaenoic acid (DHA) and inflammatory bowel disease (IBD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 401

Mediation analysis diagram illustrating the potential pathway through which docosahexaenoic acid (DHA) may influence inflammatory bowel disease (IBD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 402

Scatter plot depicting the causal effect estimates of individual genetic instruments for docosahexaenoic acid (DHA) on inflammatory bowel disease (IBD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 403

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of docosahexaenoic acid (DHA) on inflammatory bowel disease (IBD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 404

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of docosahexaenoic acid (DHA) and inflammatory bowel disease (IBD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 405

Leave-one-out sensitivity analysis for the causal relationship between docosahexaenoic acid (DHA) and inflammatory bowel disease (IBD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 406

Mediation analysis diagram illustrating the potential pathway through which docosahexaenoic acid (DHA) may influence inflammatory bowel disease (IBD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 407

Scatter plot depicting the causal effect estimates of individual genetic instruments for docosahexaenoic acid (DHA) on inflammatory bowel disease (IBD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 408

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of docosahexaenoic acid (DHA) on inflammatory bowel disease (IBD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 409

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of docosahexaenoic acid (DHA) and inflammatory bowel disease (IBD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 410

Leave-one-out sensitivity analysis for the causal relationship between docosahexaenoic acid (DHA) and inflammatory bowel disease (IBD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 411

Mediation analysis diagram illustrating the potential pathway through which docosahexaenoic acid (DHA) may influence inflammatory bowel disease (IBD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 412

Scatter plot depicting the causal effect estimates of individual genetic instruments for docosahexaenoic acid (DHA) on Crohn's disease (CD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 413

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of docosahexaenoic acid (DHA) on Crohn's disease (CD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 414

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of docosahexaenoic acid (DHA) and Crohn's disease (CD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 415

Leave-one-out sensitivity analysis for the causal relationship between docosahexaenoic acid (DHA) and Crohn's disease (CD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 416

Mediation analysis diagram illustrating the potential pathway through which docosahexaenoic acid (DHA) may influence Crohn's disease (CD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 417

Scatter plot depicting the causal effect estimates of individual genetic instruments for docosahexaenoic acid (DHA) on Crohn's disease (CD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 418

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of docosahexaenoic acid (DHA) on Crohn's disease (CD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 419

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of docosahexaenoic acid (DHA) and Crohn's disease (CD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 420

Leave-one-out sensitivity analysis for the causal relationship between docosahexaenoic acid (DHA) and Crohn's disease (CD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 421

Mediation analysis diagram illustrating the potential pathway through which docosahexaenoic acid (DHA) may influence Crohn's disease (CD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 422

Scatter plot depicting the causal effect estimates of individual genetic instruments for docosahexaenoic acid (DHA) on Crohn's disease (CD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 423

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of docosahexaenoic acid (DHA) on Crohn's disease (CD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 424

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of docosahexaenoic acid (DHA) and Crohn's disease (CD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 425

Leave-one-out sensitivity analysis for the causal relationship between docosahexaenoic acid (DHA) and Crohn's disease (CD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 426

Mediation analysis diagram illustrating the potential pathway through which docosahexaenoic acid (DHA) may influence Crohn's disease (CD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 427

Scatter plot depicting the causal effect estimates of individual genetic instruments for docosahexaenoic acid (DHA) on Crohn's disease (CD), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 428

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of docosahexaenoic acid (DHA) on Crohn's disease (CD). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 429

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of docosahexaenoic acid (DHA) and Crohn's disease (CD). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 430

Leave-one-out sensitivity analysis for the causal relationship between docosahexaenoic acid (DHA) and Crohn's disease (CD). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 431

Mediation analysis diagram illustrating the potential pathway through which docosahexaenoic acid (DHA) may influence Crohn's disease (CD) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 432

Scatter plot depicting the causal effect estimates of individual genetic instruments for docosahexaenoic acid (DHA) on ulcerative colitis (UC), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 433

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of docosahexaenoic acid (DHA) on ulcerative colitis (UC). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 434

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of docosahexaenoic acid (DHA) and ulcerative colitis (UC). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 435

Leave-one-out sensitivity analysis for the causal relationship between docosahexaenoic acid (DHA) and ulcerative colitis (UC). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 436

Mediation analysis diagram illustrating the potential pathway through which docosahexaenoic acid (DHA) may influence ulcerative colitis (UC) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 437

Scatter plot depicting the causal effect estimates of individual genetic instruments for docosahexaenoic acid (DHA) on ulcerative colitis (UC), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 438

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of docosahexaenoic acid (DHA) on ulcerative colitis (UC). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 439

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of docosahexaenoic acid (DHA) and ulcerative colitis (UC). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 440

Leave-one-out sensitivity analysis for the causal relationship between docosahexaenoic acid (DHA) and ulcerative colitis (UC). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 441

Mediation analysis diagram illustrating the potential pathway through which docosahexaenoic acid (DHA) may influence ulcerative colitis (UC) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 442

Scatter plot depicting the causal effect estimates of individual genetic instruments for docosahexaenoic acid (DHA) on ulcerative colitis (UC), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 443

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of docosahexaenoic acid (DHA) on ulcerative colitis (UC). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 444

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of docosahexaenoic acid (DHA) and ulcerative colitis (UC). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 445

Leave-one-out sensitivity analysis for the causal relationship between docosahexaenoic acid (DHA) and ulcerative colitis (UC). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 446

Mediation analysis diagram illustrating the potential pathway through which docosahexaenoic acid (DHA) may influence ulcerative colitis (UC) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 447

Scatter plot depicting the causal effect estimates of individual genetic instruments for docosahexaenoic acid (DHA) on ulcerative colitis (UC), assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 448

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of docosahexaenoic acid (DHA) on ulcerative colitis (UC). Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 449

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of docosahexaenoic acid (DHA) and ulcerative colitis (UC). Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 450

Leave-one-out sensitivity analysis for the causal relationship between docosahexaenoic acid (DHA) and ulcerative colitis (UC). Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 451

Mediation analysis diagram illustrating the potential pathway through which docosahexaenoic acid (DHA) may influence ulcerative colitis (UC) risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 452

Scatter plot depicting the causal effect estimates of individual genetic instruments for total omega-3 fatty acids on IBD and its subtypes, assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 453

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of total omega-3 fatty acids on IBD and its subtypes. Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 454

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of total omega-3 fatty acids and IBD and its subtypes. Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.

Figure 455

Leave-one-out sensitivity analysis for the causal relationship between total omega-3 fatty acids and IBD and its subtypes. Sequentially removing each genetic instrument and recalculating the pooled estimate indicates the robustness of the overall finding to any single influential variant.

Figure 456

Mediation analysis diagram illustrating the potential pathway through which total omega-3 fatty acids may influence IBD and its subtypes risk via circulating metabolites. Direct and indirect effects are quantified using two-step Mendelian randomization, highlighting metabolites that may partially mediate the observed association.

Figure 457

Scatter plot depicting the causal effect estimates of individual genetic instruments for total omega-3 fatty acids on IBD and its subtypes, assessed using Mendelian randomization. Each point represents a single SNP, with the slope reflecting the overall causal estimate.

Figure 458

Forest plot summarizing the individual and pooled Mendelian randomization estimates for the effect of total omega-3 fatty acids on IBD and its subtypes. Each horizontal line represents the causal estimate from a single genetic variant, with the diamond indicating the combined effect across multiple MR methods.

Figure 459

Funnel plot evaluating potential directional pleiotropy in the Mendelian randomization analysis of total omega-3 fatty acids and IBD and its subtypes. Asymmetry in the distribution of individual SNP estimates around the overall effect size may indicate the presence of pleiotropic bias.