Image_5_Mendelian randomization analysis reveals causal effects of food intakes on inflammatory bowel disease risk.pdf

Traditional observational studies have indicated a link between specific food intakes and inflammatory bowel disease (IBD), but the nature of such links remains unknown. We sought to assess the potential causal relationship between food intakes and IBD risk using Mendelian randomization methods. This study used summary statistics data from large-scale genome-wide association studies (GWAS) on food intakes, Crohn’s disease (CD), and ulcerative colitis (UC). In the primary analysis, we used the inverse variance-weighted method to determine whether specific food was causal for CD and UC. In addition, we also ran four other Mendelian randomization methods, including MR Egger, weighted median, maximum likelihood, and weighted mode as a complement. The primary analysis showed that high consumption of poultry (OR, 3.696; 95% CI, 1.056–12.937; p = 0.041) and cereal (OR, 2.449; 95% CI, 1.094–5.482; p = 0.029) had a significant causal association with CD, while high oily fish intake level was found to be statistically significantly associated with the risk of UC (OR, 1.482; 95% CI, 1.002–2.194; p = 0.049). This MR study provides evidence of a potential causal link between certain food intake and CD and UC.</p

Image_2_Mendelian randomization analysis reveals causal effects of food intakes on inflammatory bowel disease risk.pdf

Traditional observational studies have indicated a link between specific food intakes and inflammatory bowel disease (IBD), but the nature of such links remains unknown. We sought to assess the potential causal relationship between food intakes and IBD risk using Mendelian randomization methods. This study used summary statistics data from large-scale genome-wide association studies (GWAS) on food intakes, Crohn’s disease (CD), and ulcerative colitis (UC). In the primary analysis, we used the inverse variance-weighted method to determine whether specific food was causal for CD and UC. In addition, we also ran four other Mendelian randomization methods, including MR Egger, weighted median, maximum likelihood, and weighted mode as a complement. The primary analysis showed that high consumption of poultry (OR, 3.696; 95% CI, 1.056–12.937; p = 0.041) and cereal (OR, 2.449; 95% CI, 1.094–5.482; p = 0.029) had a significant causal association with CD, while high oily fish intake level was found to be statistically significantly associated with the risk of UC (OR, 1.482; 95% CI, 1.002–2.194; p = 0.049). This MR study provides evidence of a potential causal link between certain food intake and CD and UC.</p

Image_6_Mendelian randomization analysis reveals causal effects of food intakes on inflammatory bowel disease risk.pdf

Traditional observational studies have indicated a link between specific food intakes and inflammatory bowel disease (IBD), but the nature of such links remains unknown. We sought to assess the potential causal relationship between food intakes and IBD risk using Mendelian randomization methods. This study used summary statistics data from large-scale genome-wide association studies (GWAS) on food intakes, Crohn’s disease (CD), and ulcerative colitis (UC). In the primary analysis, we used the inverse variance-weighted method to determine whether specific food was causal for CD and UC. In addition, we also ran four other Mendelian randomization methods, including MR Egger, weighted median, maximum likelihood, and weighted mode as a complement. The primary analysis showed that high consumption of poultry (OR, 3.696; 95% CI, 1.056–12.937; p = 0.041) and cereal (OR, 2.449; 95% CI, 1.094–5.482; p = 0.029) had a significant causal association with CD, while high oily fish intake level was found to be statistically significantly associated with the risk of UC (OR, 1.482; 95% CI, 1.002–2.194; p = 0.049). This MR study provides evidence of a potential causal link between certain food intake and CD and UC.</p

Image_7_Mendelian randomization analysis reveals causal effects of food intakes on inflammatory bowel disease risk.pdf

Traditional observational studies have indicated a link between specific food intakes and inflammatory bowel disease (IBD), but the nature of such links remains unknown. We sought to assess the potential causal relationship between food intakes and IBD risk using Mendelian randomization methods. This study used summary statistics data from large-scale genome-wide association studies (GWAS) on food intakes, Crohn’s disease (CD), and ulcerative colitis (UC). In the primary analysis, we used the inverse variance-weighted method to determine whether specific food was causal for CD and UC. In addition, we also ran four other Mendelian randomization methods, including MR Egger, weighted median, maximum likelihood, and weighted mode as a complement. The primary analysis showed that high consumption of poultry (OR, 3.696; 95% CI, 1.056–12.937; p = 0.041) and cereal (OR, 2.449; 95% CI, 1.094–5.482; p = 0.029) had a significant causal association with CD, while high oily fish intake level was found to be statistically significantly associated with the risk of UC (OR, 1.482; 95% CI, 1.002–2.194; p = 0.049). This MR study provides evidence of a potential causal link between certain food intake and CD and UC.</p

Image_4_Mendelian randomization analysis reveals causal effects of food intakes on inflammatory bowel disease risk.pdf

Traditional observational studies have indicated a link between specific food intakes and inflammatory bowel disease (IBD), but the nature of such links remains unknown. We sought to assess the potential causal relationship between food intakes and IBD risk using Mendelian randomization methods. This study used summary statistics data from large-scale genome-wide association studies (GWAS) on food intakes, Crohn’s disease (CD), and ulcerative colitis (UC). In the primary analysis, we used the inverse variance-weighted method to determine whether specific food was causal for CD and UC. In addition, we also ran four other Mendelian randomization methods, including MR Egger, weighted median, maximum likelihood, and weighted mode as a complement. The primary analysis showed that high consumption of poultry (OR, 3.696; 95% CI, 1.056–12.937; p = 0.041) and cereal (OR, 2.449; 95% CI, 1.094–5.482; p = 0.029) had a significant causal association with CD, while high oily fish intake level was found to be statistically significantly associated with the risk of UC (OR, 1.482; 95% CI, 1.002–2.194; p = 0.049). This MR study provides evidence of a potential causal link between certain food intake and CD and UC.</p

Image_1_Mendelian randomization analysis reveals causal effects of food intakes on inflammatory bowel disease risk.pdf

Traditional observational studies have indicated a link between specific food intakes and inflammatory bowel disease (IBD), but the nature of such links remains unknown. We sought to assess the potential causal relationship between food intakes and IBD risk using Mendelian randomization methods. This study used summary statistics data from large-scale genome-wide association studies (GWAS) on food intakes, Crohn’s disease (CD), and ulcerative colitis (UC). In the primary analysis, we used the inverse variance-weighted method to determine whether specific food was causal for CD and UC. In addition, we also ran four other Mendelian randomization methods, including MR Egger, weighted median, maximum likelihood, and weighted mode as a complement. The primary analysis showed that high consumption of poultry (OR, 3.696; 95% CI, 1.056–12.937; p = 0.041) and cereal (OR, 2.449; 95% CI, 1.094–5.482; p = 0.029) had a significant causal association with CD, while high oily fish intake level was found to be statistically significantly associated with the risk of UC (OR, 1.482; 95% CI, 1.002–2.194; p = 0.049). This MR study provides evidence of a potential causal link between certain food intake and CD and UC.</p

Image_3_Mendelian randomization analysis reveals causal effects of food intakes on inflammatory bowel disease risk.pdf

Traditional observational studies have indicated a link between specific food intakes and inflammatory bowel disease (IBD), but the nature of such links remains unknown. We sought to assess the potential causal relationship between food intakes and IBD risk using Mendelian randomization methods. This study used summary statistics data from large-scale genome-wide association studies (GWAS) on food intakes, Crohn’s disease (CD), and ulcerative colitis (UC). In the primary analysis, we used the inverse variance-weighted method to determine whether specific food was causal for CD and UC. In addition, we also ran four other Mendelian randomization methods, including MR Egger, weighted median, maximum likelihood, and weighted mode as a complement. The primary analysis showed that high consumption of poultry (OR, 3.696; 95% CI, 1.056–12.937; p = 0.041) and cereal (OR, 2.449; 95% CI, 1.094–5.482; p = 0.029) had a significant causal association with CD, while high oily fish intake level was found to be statistically significantly associated with the risk of UC (OR, 1.482; 95% CI, 1.002–2.194; p = 0.049). This MR study provides evidence of a potential causal link between certain food intake and CD and UC.</p

Image_8_Mendelian randomization analysis reveals causal effects of food intakes on inflammatory bowel disease risk.pdf

Traditional observational studies have indicated a link between specific food intakes and inflammatory bowel disease (IBD), but the nature of such links remains unknown. We sought to assess the potential causal relationship between food intakes and IBD risk using Mendelian randomization methods. This study used summary statistics data from large-scale genome-wide association studies (GWAS) on food intakes, Crohn’s disease (CD), and ulcerative colitis (UC). In the primary analysis, we used the inverse variance-weighted method to determine whether specific food was causal for CD and UC. In addition, we also ran four other Mendelian randomization methods, including MR Egger, weighted median, maximum likelihood, and weighted mode as a complement. The primary analysis showed that high consumption of poultry (OR, 3.696; 95% CI, 1.056–12.937; p = 0.041) and cereal (OR, 2.449; 95% CI, 1.094–5.482; p = 0.029) had a significant causal association with CD, while high oily fish intake level was found to be statistically significantly associated with the risk of UC (OR, 1.482; 95% CI, 1.002–2.194; p = 0.049). This MR study provides evidence of a potential causal link between certain food intake and CD and UC.</p