Clinical and translational gastroenterology · 2026
Plasma Phospholipids and Incident Ulcerative Colitis: A Prospective Cohort Study in the UK Biobank.
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Tang Jialu, Zhou Dawei, Liu Shaojun
Аннотация
INTRODUCTION: To investigate the association between plasma levels of total phospholipids in lipoprotein particles and the risk of incident ulcerative colitis (UC).
METHODS: This prospective cohort study analyzed data from 254,921 participants in the UK Biobank (2006-2020), excluding those with preexisting UC or missing data. Phospholipid levels were measured by nuclear magnetic resonance spectroscopy. Cox proportional hazards models were adjusted for demographic, lifestyle, socioeconomic, and genetic factors. Dose-response and subgroup analyses were conducted using generalized additive models.
RESULTS: During a median follow-up duration of 15.78 years, 1,330 incident UC cases were identified. Higher phospholipid levels demonstrated a significant inverse association with UC risk. After full adjustment, each unit increase in phospholipids was associated with a 16% lower risk (hazard ratio 0.84, 95% confidence interval 0.75-0.95, P = 0.006). Quartile analyses showed lower risks in higher quartiles, with the risk reduction most evident by the third quartile and then generally stable (Q4 vs Q1: hazard ratio 0.83, 95% confidence interval 0.71-0.97, P = 0.020). Generalized additive and quartile analyses suggested a nonlinear plateau/threshold pattern rather than a strictly linear association. Subfraction analyses showed heterogeneous associations, with inverse patterns mainly observed for phospholipids carried by high-density lipoprotein cholesterol, intermediate-density lipoprotein, and low-density lipoprotein cholesterol particles, whereas chylomicron- and several very low-density lipoprotein-related phospholipids showed null or positive/nonprotective associations.
DISCUSSION: Higher plasma total phospholipid levels are independently associated with reduced UC risk, suggesting phospholipid metabolism may play a protective role in UC pathogenesis. However, this association is not uniform across lipoprotein subfractions. These findings highlight potential metabolic biomarkers and mechanistic pathways requiring further validation for UC prevention.
METHODS: This prospective cohort study analyzed data from 254,921 participants in the UK Biobank (2006-2020), excluding those with preexisting UC or missing data. Phospholipid levels were measured by nuclear magnetic resonance spectroscopy. Cox proportional hazards models were adjusted for demographic, lifestyle, socioeconomic, and genetic factors. Dose-response and subgroup analyses were conducted using generalized additive models.
RESULTS: During a median follow-up duration of 15.78 years, 1,330 incident UC cases were identified. Higher phospholipid levels demonstrated a significant inverse association with UC risk. After full adjustment, each unit increase in phospholipids was associated with a 16% lower risk (hazard ratio 0.84, 95% confidence interval 0.75-0.95, P = 0.006). Quartile analyses showed lower risks in higher quartiles, with the risk reduction most evident by the third quartile and then generally stable (Q4 vs Q1: hazard ratio 0.83, 95% confidence interval 0.71-0.97, P = 0.020). Generalized additive and quartile analyses suggested a nonlinear plateau/threshold pattern rather than a strictly linear association. Subfraction analyses showed heterogeneous associations, with inverse patterns mainly observed for phospholipids carried by high-density lipoprotein cholesterol, intermediate-density lipoprotein, and low-density lipoprotein cholesterol particles, whereas chylomicron- and several very low-density lipoprotein-related phospholipids showed null or positive/nonprotective associations.
DISCUSSION: Higher plasma total phospholipid levels are independently associated with reduced UC risk, suggesting phospholipid metabolism may play a protective role in UC pathogenesis. However, this association is not uniform across lipoprotein subfractions. These findings highlight potential metabolic biomarkers and mechanistic pathways requiring further validation for UC prevention.