Body weight variability and the risk of cardiovascular outcomes in patients with nonalcoholic fatty liver disease.
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ABSTRACT:
SUBMITTER: Kim MN
PROVIDER: S-EPMC8080815 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Weight loss, the most established therapy for nonalcoholic fatty liver disease (NAFLD), is frequently followed by weight regain and fluctuation. The aim of this study was to investigate whether body weight change and variability were independent risk factors for incident NAFLD. We conducted a longitudinal cohort study. Among the 1907 participants, incident NAFLD occurred in 420 (22.0%) cases during median follow-up of 5.6 years. In the multivariate analysis, there was no significant association between weight variability and the risk of incident NAFLD. The risk of incident NAFLD was significantly higher in subjects with weight gain ≥ 10% and 7% < gain ≤ 10% [hazard ratios (HR), 2.43; 95% confidence intervals (CI), 1.65-3.58 and HR, 1.73; 95% CI, 1.26-2.39, respectively], while the risk of incident NAFLD was significantly lower in those with -7% < weight loss ≤ --3% (HR, 0.33; 95% CI, 0.22-0.51). Overall body weight gain rather than bodyweight variability was independently associated with the risk of incident NAFLD. Understanding the association between body weight variability and incident NAFLD may have future clinical implications for the quantification of weight loss as a treatment for patients with NAFLD.
| S-EPMC8277820 | biostudies-literature
Project description:BackgroundWeight loss through lifestyle modification is recommended for patients with nonalcoholic fatty liver disease (NAFLD). Recent studies have suggested that repeated loss and gain of weight is associated with worse health outcomes. This study aimed to examine the association between weight variability and the risk of NAFLD in patients without diabetes.MethodsWe examined the health-checkup data of 30,708 participants who had undergone serial examinations between 2010 and 2014. Weight variability was assessed using coefficient of variation and the average successive variability of weight (ASVW), which was defined as the sum of absolute weight changes between successive years over the 5-year period divided by 4. The participants were classified according to the baseline body mass index and weight difference over 4 years.ResultsOn dividing the participants into four groups according to ASVW quartile groups, those in the highest quartile showed a significantly increased risk of NAFLD compared to those in the lowest quartile (odds ratio [OR], 1.89; 95% confidence interval [CI], 1.63 to 2.19). Among participants without obesity at baseline, individuals with high ASVW showed increased risk of NAFLD (OR, 1.80; 95% CI, 1.61 to 2.01). Participants with increased weight over 4 years and high ASVW demonstrated higher risk of NAFLD compared to those with stable weight and low ASVW (OR, 4.87; 95% CI, 4.29 to 5.53).ConclusionRegardless of participant baseline obesity status, high weight variability was associated with an increased risk of developing NAFLD. Our results suggest that further effort is required to minimize weight fluctuations after achieving a desirable body weight.
| S-EPMC8419611 | biostudies-literature
Project description:This study aimed to determine whether nonalcoholic fatty liver disease (NAFLD) is an independent risk factor for CVD and to identify the most useful NAFLD diagnostic tool for predicting CVD. Data from a total of 23,376 Korean adults without established CVD were analyzed. Cardiovascular risk was calculated using the Framingham Risk Score (FRS) 2008. The presence of NAFLD was defined as moderate-to-severe fatty liver disease diagnosed by ultrasonography. Scores for fatty liver were calculated using four NAFLD scoring systems (Fatty Liver Index, FLI; Hepatic Steatosis Index, HSI; Simple NAFLD Score, SNS; Comprehensive NAFLD Score, CNS), and were compared and analyzed according to cardiovascular risk group. Using the FRS, 67.4% of participants were considered to be at low risk of CVD, 21.5% at intermediate risk, and 11.1% at high risk. As the risk of CVD increased, both the prevalence of NAFLD and the score from each NAFLD scoring system increased significantly (p < 0.001). In the unadjusted analysis, the CNS had the strongest association with high CVD risk; in the adjusted analysis, the FLI score was most strongly associated with high CVD risk. Fatty liver is an important independent risk factor for CVD. Therefore, the available NAFLD scoring systems could be utilized to predict CVD.
| S-EPMC8303122 | biostudies-literature
Project description:Nonalcoholic fatty liver disease is increasingly recognized as a major global health problem. Intertwined with diabetes, metabolic syndrome, and obesity, nonalcoholic fatty liver disease embraces a spectrum of liver conditions spanning from steatosis to inflammation, fibrosis, and liver failure. Compared with the general population, the prevalence of cardiovascular disease is higher among nonalcoholic fatty liver disease patients, in whom comprehensive cardiovascular risk assessment is highly desirable. Preclinical effects of nonalcoholic fatty liver disease on the heart include both metabolic and structural changes eventually preceding overt myocardial dysfunction. Particularly, nonalcoholic fatty liver disease is associated with enhanced atherosclerosis, heart muscle disease, valvular heart disease, and arrhythmias, with endothelial dysfunction, inflammation, metabolic dysregulation, and oxidative stress playing in the background. In this topical review, we aimed to summarize current evidence on the epidemiology of nonalcoholic fatty liver disease, discuss the pathophysiological links between nonalcoholic fatty liver disease and cardiovascular disease, illustrate nonalcoholic fatty liver disease-related cardiovascular phenotypes, and finally provide a glimpse on the relationship between nonalcoholic fatty liver disease and cardiac steatosis, mitochondrial (dys)function, and cardiovascular autonomic dysfunction.
| S-EPMC7307287 | biostudies-literature
Project description:BACKGROUND & AIMS:Cardiovascular disease (CVD) is the leading cause of death among patients with nonalcoholic fatty liver disease (NAFLD). Moderate drinking (vs abstinence) is associated with lower risk of CVD in the general population. We assessed whether alcohol use is associated with CVD risk in patients with NAFLD. METHODS:We analyzed data from participants in the Coronary Artery Risk Development in Young Adults longitudinal cohort study of 5115 black and white young adults, 18-30 years old, recruited from 4 cities in the United States from 1985 through 1986. Participants self-reported alcohol use at study entry and then again after 15, 20, and 25 years. At year 25 (2010-2011), participants underwent computed tomography examination of the thorax and abdomen and tissue Doppler echocardiography with myocardial strain measured by speckle tracking. Coronary artery calcification was defined as an Agatston score above 0. NAFLD was defined as liver attenuation <51 Hounsfield Units after exclusions. Drinkers reported 1-21 (men) or 1-14 (women) standard drinks/week at years 15, 20, or 25. Nondrinkers reported no alcohol use at years 15, 20, and 25. RESULTS:Of the 570 participants with NAFLD (mean age, 50 years; 54% black; 46% female), 332 (58%) were drinkers; significantly higher proportions of drinkers were white, male, and with higher levels of education compared with nondrinkers (P < .05 for all). Higher proportions of drinkers had obesity, diabetes, and metabolic syndrome compared with nondrinkers (P < .01). There was no difference in liver attenuation between groups (P = .12). After multivariable adjustment, there was no association between alcohol use and CVD risk factors (diabetes, hypertension, hyperlipidemia) or subclinical CVD measures (coronary artery calcification, early transmitral velocity/late (atrial) transmitral velocity (E/A) ratio, global longitudinal strain). CONCLUSIONS:In a population-based sample of individuals with NAFLD in midlife, prospectively assessed alcohol use is not associated with significant differences in risk factors for CVD or markers of subclinical CVD. In contrast to general population findings, alcohol use may not reduce the risk of CVD in patients with NAFLD.
| S-EPMC5669829 | biostudies-literature
Project description:Nonalcoholic fatty liver disease is now regarded as the most common form of chronic liver disease in adults and children. The close association between nonalcoholic fatty liver disease (NAFLD) and the metabolic syndrome has been extensively described. Moreover, a growing body of evidence suggest that NAFLD by itself confers a substantial cardiovascular risk independent of the other components of the metabolic syndrome. Given the significant potential for morbidity and mortality in these patients, and the large proportion of both pediatric and adult population affected, it is important that we clearly define the overall risk, identify early predictors for cardiovascular disease progression, and establish management strategies. In this article, we will focus on current data linking NAFLD and the severity of liver damage present in children with cardiovascular risk.
| S-EPMC3234131 | biostudies-literature
Project description:Cardiovascular diseases (CVDs) are the leading cause of mortality in patients with nonalcoholic fatty liver disease (NAFLD). Our aim was to assess the association of atherosclerotic cardiovascular disease (ASCVD) risk scores with overall and cardiac-specific mortality among patients with NAFLD. We used the National Health and Nutrition Examination Survey III with the National Death Index-linked mortality files. NAFLD was defined by ultrasound as presence of steatosis in the absence of secondary causes of liver disease. High risk for CVD was defined as a 10-year ASCVD score ≥7.5%. Hazard ratios (HRs) and population-attributable fractions (PAFs) of high risk for CVD were calculated. Among 1,262 subjects with NAFLD (47.9% men; 41.2% white; mean age, 56.3 years), the prevalence of high risk for CVD was 55.9% and 4.8% had advanced fibrosis. After a median follow-up of 17.7 years, 482 subjects (38.2%) died of overall causes, of whom 382 (79.3%) had a high risk for CVD. The unadjusted overall and cardiac-specific mortality were higher for patients with NAFLD who had a high risk for CVD compared to subjects with NAFLD with a low risk for CVD (57.3% vs. 16.8% for overall mortality; 16.4% vs. 3.5% for cardiovascular mortality). After controlling for risk factors associated with mortality, high risk for CVD was associated with a 42% higher overall mortality rate (adjusted HR [aHR], 1.42; 95% confidence interval [CI], 1.05-1.91) and twice the risk of cardiovascular mortality (aHR, 2.02; 95% CI, 1.12-3.65). Adjusted PAFs were 11.4% for overall mortality and 44.9% for cardiovascular mortality. Conclusion: Among patients with NAFLD, ASCVD score ≥7.5% was associated with a higher risk of overall and cardiac-specific mortality.
| S-EPMC6671783 | biostudies-literature
Project description:Up to 25% of patients with nonalcoholic fatty liver disease (NAFLD) are not obese but may have a fat or muscle composition that predisposes them to NAFLD. Our aim was to determine whether body composition parameters associate with NAFLD and to identify genetic contributors to this association. This study included two cohorts. The first included 2,249 participants from the Framingham Heart Study who underwent a computed tomography scan to evaluate hepatic steatosis, dual-energy x-ray absorptiometry testing to assess body composition, and clinical examination. Body composition parameters were normalized to total body weight. A subset of participants underwent genotyping with an Affymetrix 550K single-nucleotide polymorphism array. The second cohort, Michigan Genomics Initiative, included 19,239 individuals with genotyping on the Illumina HumanCoreExome v.12.1 array and full electronic health record data. Using sex-stratified multivariable linear regression, greater central body fat associated with increased hepatic steatosis while greater lower extremity body fat associated with decreased hepatic steatosis. Greater appendicular lean mass was associated with decreased hepatic steatosis in men but not in women. A polygenic risk score for lipodystrophy (regional or global loss of adipose tissue) was associated with increased hepatic steatosis, increased liver fibrosis, and decreased lower extremity fat mass. Conclusion: Greater central body fat associated with increased hepatic steatosis, while greater lower extremity body fat and, in men, greater appendicular lean mass were associated with decreased hepatic steatosis. A genetic risk score for lipodystrophy was associated with NAFLD and liver fibrosis. Our results suggest that buffering of excess energy by peripheral fat and muscle may protect against NAFLD and liver fibrosis in the general population.
| S-EPMC6671828 | biostudies-literature
Project description:Background & aimsAlthough primarily a disease with liver-specific complications, nonalcoholic fatty liver disease (NAFLD) is a systemic disease with extrahepatic complications. We aim to evaluate the association between NAFLD and cardiovascular disease (CVD), stroke and cerebrovascular disease, and extrahepatic cancers.MethodsWe searched MEDLINE, EMBASE, and Cochrane Systematic Review Database from January 1, 2000 to July 1, 2019 to identify peer-reviewed English language literature using predefined keywords for NAFLD, CVD, stroke and cerebrovascular disease, and extrahepatic cancers among adults. Two reviewers independently selected studies for inclusion. Measures of association between NAFLD and CVD, stroke and cerebrovascular disease, and extrahepatic cancers were extracted. Quality assessed using Newcastle-Ottawa scale and Grading of Recommendations Assessment, Development and Evaluation (GRADE).ResultsThirty studies were included evaluating CVD, 16 studies evaluating stroke or cerebrovascular disease, and 13 studies evaluating extrahepatic cancers. On pooled meta-analysis assessment, NAFLD was associated with increased risk of CVD (risk ratio [RR]: 1.78; 95% confidence interval [CI]: 1.52-2.08) and stroke or cerebrovascular disease (RR: 2.08, 95% CI: 1.72-2.51). Significant heterogeneity in assessing extrahepatic cancers prevented applying meta-analysis methods, but NAFLD seemed to be associated with increased risk of breast and colorectal cancers. Overall level of quality of studies were very low by GRADE.ConclusionsNAFLD is associated with increased risks of CVD and stroke or cerebrovascular disease among adults. There appears to be increased risk of breast and colorectal cancers. Given low quality of evidence, it is premature to make any strong conclusions to modify CVD, stroke, or cancer screening policies in patients with NAFLD.
| S-EPMC7897860 | biostudies-literature
Project description:This study evaluated the effect of weight loss on pediatric nonalcoholic fatty liver disease (NAFLD). Subjects included 81 overweight NAFLD patients referred to two pediatric gastroenterologists from 2000 to 2010. Data on subjects were obtained from review of medical charts. The effect of weight loss was assessed at 1-4?months, 5-8?months, 9-12?months, and beyond one year as the change in weight, BMI z-score (for age-and-sex), and alanine aminotransferase and the relationship between the change in body weight and BMI z-score, and the change in alanine aminotransferase. Subjects were mostly obese (99%), male (86%), and Asian (63%) and had median age of 14.1 (11.2-16.2)?years and alanine aminotransferase of 105 (78-153) U/L at referral. Alanine aminotransferase decreased 32?±?66 (P = 0.016), 30?±?65 (P = 0.134), 37?±?75 (P = 0.0157), and 45?±?69 (P = 0.014) for subjects with follow-up data at 1-4?months (n = 47), 5-8?months (n = 26), 9-12 months (n = 19), and beyond one year (n = 19), respectively. During these time periods, neither was body weight (-0.2 to +7.1?kg) or BMI z-score (-0.12 to -0.05) significantly reduced, nor were changes in these variables associated with the change in alanine aminotransferase. These findings suggest that weight and BMI z-score may not be sufficient indicators of treatment response in pediatric NAFLD patients.
| S-EPMC3678446 | biostudies-literature