Association between dietary fatty acids and all-cause mortality in patients with cirrhosis: A cohort study.

IF 3 4区 医学 Q2 PHYSIOLOGY
Ali Jafari, Ghazaleh Mahdavi-Mazdeh, Behnaz Narimani, Helia Mardani, Azita Hekmatdoost, Fereshteh Pashayee-Khamene, Sara Karimi, Saleheh Ahmadzadeh, Mehdi Saberifiroozi, Behzad Hatami, Zahra Yari
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Abstract

Liver cirrhosis imposes a substantial global burden, with complications driving high mortality. Diet is pivotal in managing liver disease progression and cirrhosis-related death. This study investigated associations between total fat intake, specific dietary fatty acid subclasses and all-cause mortality in cirrhotic patients. In this prospective cohort study, 121 ambulatory patients with recently diagnosed cirrhosis (≤6 months) were enrolled. Baseline dietary intake was evaluated via a validated 168-item semi-quantitative food frequency questionnaire. Participants were categorized into tertiles by total fat and fatty acid subclasses: saturated (SFA), monounsaturated (MUFA), polyunsaturated (PUFA), omega-3 and omega-6 fatty acids. Cox proportional hazards models computed hazard ratios (HRs) and 95% confidence intervals (CIs), adjusted sequentially for age, sex, energy intake, BMI, smoking, alcohol use, cirrhosis aetiology, MELD score and Child-Pugh class. During the 60-month follow-up, 50 deaths (41.3%) occurred. In fully adjusted models, highest versus lowest tertiles of total fat intake (HR = 6.69; 95% CI: 1.37-13.34; P-trend = 0.017), SFA intake (HR = 8.2; 95% CI: 1.33-20.53; P-trend = 0.014) and PUFA-6 intake (HR = 5.24; 95% CI: 1.1-26.44; P-trend = 0.014) were independently associated with significantly elevated mortality risk. No significant associations were observed for MUFA, total PUFA or PUFA-3 intake. Kaplan-Meier analyses confirmed significantly reduced 5-year survival with higher total fat (log-rank P = 0.003) and SFA intake (log-rank P < 0.001). In this exploratory prospective cohort study, higher intakes of total fat, saturated fatty acids and omega-6 polyunsaturated fatty acids were associated with increased all-cause mortality among patients with cirrhosis. These preliminary findings are hypothesis-generating and require confirmation in larger, adequately powered prospective studies.

肝硬化患者膳食脂肪酸与全因死亡率之间的关系:一项队列研究。
肝硬化是一项重大的全球负担,其并发症导致高死亡率。饮食是控制肝病进展和肝硬化相关死亡的关键。本研究调查了肝硬化患者总脂肪摄入量、特定膳食脂肪酸亚类和全因死亡率之间的关系。在这项前瞻性队列研究中,121例新近诊断为肝硬化(≤6个月)的门诊患者入组。基线膳食摄入量通过一份包含168项的半定量食物频率问卷进行评估。参与者按总脂肪和脂肪酸亚类分为三类:饱和(SFA)、单不饱和(MUFA)、多不饱和(PUFA)、omega-3和omega-6脂肪酸。Cox比例风险模型计算了风险比(hr)和95%置信区间(ci),并根据年龄、性别、能量摄入、BMI、吸烟、饮酒、肝硬化病因、MELD评分和Child-Pugh分级进行了顺序调整。在60个月的随访期间,发生50例死亡(41.3%)。在完全调整后的模型中,总脂肪摄入量(HR = 6.69; 95% CI: 1.37-13.34; P-trend = 0.017)、SFA摄入量(HR = 8.2; 95% CI: 1.33-20.53; P-trend = 0.014)和PUFA-6摄入量(HR = 5.24; 95% CI: 1.1-26.44; P-trend = 0.014)与死亡风险显著升高独立相关。未观察到多聚脂肪酸、总多聚脂肪酸或多聚脂肪酸-3摄入量之间的显著关联。Kaplan-Meier分析证实,总脂肪(log-rank P = 0.003)和SFA摄入量(log-rank P = 0.003)的增加显著降低了5年生存率
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来源期刊
Experimental Physiology
Experimental Physiology 医学-生理学
CiteScore
5.10
自引率
3.70%
发文量
262
审稿时长
1 months
期刊介绍: Experimental Physiology publishes research papers that report novel insights into homeostatic and adaptive responses in health, as well as those that further our understanding of pathophysiological mechanisms in disease. We encourage papers that embrace the journal’s orientation of translation and integration, including studies of the adaptive responses to exercise, acute and chronic environmental stressors, growth and aging, and diseases where integrative homeostatic mechanisms play a key role in the response to and evolution of the disease process. Examples of such diseases include hypertension, heart failure, hypoxic lung disease, endocrine and neurological disorders. We are also keen to publish research that has a translational aspect or clinical application. Comparative physiology work that can be applied to aid the understanding human physiology is also encouraged. Manuscripts that report the use of bioinformatic, genomic, molecular, proteomic and cellular techniques to provide novel insights into integrative physiological and pathophysiological mechanisms are welcomed.
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