Population Sciences Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland; Framingham Heart Study, Framingham, Massachusetts.
Section of Gastroenterology, Evans Department of Medicine, Boston University School of Medicine, Boston, Massachusetts.
Gastroenterology. 2018 Jul;155(1):107-117. doi: 10.1053/j.gastro.2018.03.038. Epub 2018 Mar 29.
BACKGROUND & AIMS: Dietary modification has been recommended for treatment of nonalcoholic fatty liver disease (NAFLD), although it is not clear whether improving diet quality can prevent its development. We performed a prospective study to examine the association between diet quality change and change in liver fat. We also examined the association between genetic risk score and liver fat change in individuals with different levels of diet quality change.
Our study included 1521 participants who attended the seventh and eighth examinations (1998-2001 and 2005-2008) of the second-generation cohort or attended the first and second examinations (2002-2005 and 2008-2011) of the third-generation cohort in the Framingham Heart Study. The self-administered semiquantitative 126-item Harvard food frequency questionnaire was used to determine dietary intake in the year leading up to an examination. We assessed levels of liver fat using liver-phantom ratio (LPR) on computed tomography images from 2002 through 2005 and again from 2008 through 2011. LPR values are inversely related to liver fat: increased LPR indicates decreased liver fat. We examined associations of changes in 2 diet scores, the Mediterranean-style diet score (MDS) and Alternative Healthy Eating Index (AHEI), with changes in liver fat and new-onset fatty liver. We evaluated interactions between diet score change and a weighted genetic risk score for NAFLD, determined based on multiple single-nucleotide polymorphisms identified in genome-wide association studies of NAFLD. The primary outcome was change in LPR between baseline and follow-up measurement.
For each 1 standard deviation increase in MDS, the LPR increased (meaning liver fat decreased) by 0.57 (95% confidence interval [CI] 0.27-0.86; P < .001) and the odds for incident fatty liver decreased by 26% (95% CI 10%-39%; P = .002). For each 1 standard deviation increase in AHEI, LPR increased by 0.56 (95% CI 0.29-0.84; P < .001) and the odds for incident fatty liver decreased by 21% (95% CI 5%-35%; P = .02). Increased diet scores were also associated with reduced odds of developing more-advanced fatty liver. Higher genetic risk scores were associated with increased liver fat accumulation in participants who had decreased MDS (P < .001) or AHEI scores (P = .001), but not in those with stable or improved diet scores (P for gene-diet interaction <.001).
In an analysis of participants in the Framingham Heart Study, increasing diet quality, determined based on MDS and AHEI scores, is associated with less liver fat accumulation and reduced risk for new-onset fatty liver. An improved diet is particularly important for individuals with a high genetic risk for NAFLD.
饮食调整已被推荐用于治疗非酒精性脂肪肝(NAFLD),尽管尚不清楚改善饮食质量是否能预防其发生。我们进行了一项前瞻性研究,以检验饮食质量变化与肝脂肪变化之间的关联。我们还检验了在不同饮食质量变化水平的个体中,遗传风险评分与肝脂肪变化之间的关联。
我们的研究包括参加弗雷明汉心脏研究第二代队列的第 7 次和第 8 次检查(1998-2001 年和 2005-2008 年)或参加第三代队列的第 1 次和第 2 次检查(2002-2005 年和 2008-2011 年)的 1521 名参与者。通过自我管理的半定量 126 项哈佛食物频率问卷来确定检查前一年的饮食摄入量。我们使用肝脏-幻影比率(LPR)在 2002 年至 2005 年和 2008 年至 2011 年期间的计算机断层扫描图像上评估肝脂肪水平。LPR 值与肝脂肪呈反比:LPR 增加表示肝脂肪减少。我们检验了两种饮食评分(地中海式饮食评分(MDS)和替代健康饮食指数(AHEI))的变化与肝脂肪变化和新发脂肪肝之间的关联。我们评估了饮食评分变化与基于 NAFLD 全基因组关联研究中确定的多个单核苷酸多态性的加权 NAFLD 遗传风险评分之间的相互作用。主要结局是基线和随访测量之间的 LPR 变化。
MDS 每增加 1 个标准差,LPR 增加(意味着肝脂肪减少)0.57(95%置信区间 [CI] 0.27-0.86;P < 0.001),新发脂肪肝的几率降低 26%(95% CI 10%-39%;P = 0.002)。AHEI 每增加 1 个标准差,LPR 增加 0.56(95% CI 0.29-0.84;P < 0.001),新发脂肪肝的几率降低 21%(95% CI 5%-35%;P = 0.02)。更高的饮食评分也与减少发生更严重脂肪肝的几率有关。较高的遗传风险评分与 MDS(P < 0.001)或 AHEI 评分降低的参与者中肝脂肪堆积增加相关(P = 0.001),但与饮食评分稳定或改善的参与者无关(P 对于基因-饮食相互作用<0.001)。
在对弗雷明汉心脏研究参与者的分析中,基于 MDS 和 AHEI 评分确定的饮食质量提高与肝脂肪积累减少和新发脂肪肝风险降低相关。对于具有 NAFLD 遗传高风险的个体,改善饮食尤为重要。