Association between obesity and non-alcoholic fatty liver disease (NAFLD) in adults aged 18 years and above - data from NHANES 2017-2018.

Reply

Nonalcoholic Fatty Liver Disease and Cardiovascular Disease Risk

Prevalence of Elevated Alanine Aminotransferase Among US Adolescents and Associated Factors: NHANES 1999–2004

Contribution of metabolic factors to alanine aminotransferase activity in persons with other causes of liver disease

NAFLD vs. MAFLD – It is not the name but the disease that decides the outcome in fatty liver

Common Genetic Variants and Nonalcoholic Fatty Liver Disease

While previous studies have identified a relationship between dietary intake and the risk of non-alcoholic fatty liver disease (NAFLD), the influence of overall nutritional status on NAFLD development has not been thoroughly investigated. This study sought to explore the association between different nutritional status indicators and NAFLD among the older adults. Nutritional status was evaluated using controlling nutritional status (CONUT), prognostic nutritional index (PNI) and nutritional risk index (GNRI), while NAFLD was identified based on a controlled attenuation parameter ≥ 285 dB/m, measured using transient elastography. The analysis included multivariate regression, receiver operating characteristic analysis, eXtreme Gradient Boosting and subgroup analysis to investigate the relationships between nutritional status indices and NAFLD. The study enrolled 1409 participants for the main analysis, with an NAFLD prevalence of 44·7 %. After accounting for potential confounders, a positive association between PNI and NAFLD was observed. Participants in the third and fourth quartiles of PNI showed increased odds of NAFLD compared with the lowest quartile (Q3: OR = 1·45, 95 % CI (1·03, 2·05); Q4: OR = 2·27, 95 % CI (1·59, 3·24)). Similarly, higher GNRI quartiles were significantly associated with greater odds of NAFLD (Q4 v. Q1: aOR = 1·84; 95 % CI (1·28, 2·65)). Conversely, higher CONUT values were linked to a reduced prevalence of NAFLD (OR = 0·65, 95 % CI (0·48, 0·87)). This study highlights that suboptimal nutritional status, indicating overnutrition as evaluated by PNI, GNRI and CONUT, is positively linked with the risk of NAFLD in individuals aged 50 years and above.

There is evidence that perfluoroalkyl substances (PFASs) have effects on liver toxicity, and the effects may exhibit sex differences. Our study aims to explore the association between exposure to four PFASs (perfluorooctanoic acid, PFOA; perfluorooctane sulfonate, PFOS; perfluorohexane sulfonate, PFHxS; and perfluorononanoate, PFNA) and the risk of nonalcoholic fatty liver disease (NAFLD) in adults ≥ 20years old in the US population. The data were based on the National Health and Nutrition Examination Survey (NHANES) 2005-2018. We used Poisson regression to explore the association between the four PFASs and NAFLD. We included 3464 participants; of these, 1200 (34.64%) individuals were defined as having NAFLD, and the prevalence of NAFLD was 39.52% in men and 30.40% in women. After Poisson regression, among the premenopausal and postmenopausal and total women, PFOA had a significantly positive association with NAFLD (p < 0.05). After principal component analysis, the "composite PFAS" was associated with NAFLD in postmenopausal and total women, and the RRs (95% CIs) were 1.306 (1.075, 1.586) and 1.161 (1.007, 1.339), respectively. In adults, we found that PFASs were associated with NAFLD, and the associations varied by sex, particularly for PFOA and PFNA, which had a positive association with NAFLD in women.

Nonalcoholic fatty liver disease (NAFLD) and infection with hepatitis B virus (HBV) or hepatitis C virus (HCV) are major causes of liver disease in adults. However, data for children and adolescents are limited. Our study aimed to characterize the prevalence, trend, and risk factors of infection of HBV and HCV and possible NAFLD for this population. We analyzed 6,647 children and adolescents (aged 6-21 years) from the 1999-2016 National Health and Nutrition Examination Survey. Among individuals aged 6-21 years, HBV prevalence decreased after 2011, from 0.72% in 1999-2004 and 0.85% in 2005-2010 to 0.27% in 2011-2016 (P < 0.001), whereas HCV prevalence increased to 0.26% in 2011-2016 after an initial decline from 0.15% in 1999-2004 to 0.02% in 2005-2010 (P = 0.01). Possible NAFLD prevalence also increased by approximately 40% in individuals aged 12-21 years, from 8.54% in 1999-2004 to 10.1% in 2005-2010 and then 11.8% in 2011-2016 (P = 0.033), with most possible NAFLD individuals being male, being obese, or having higher glucose, fasting insulin, hemoglobin A1c, homeostatic model assessment of insulin resistance, liver enzymes, lipids, and uric acid (all P < 0.01). On multivariate logistic regression, hypertension (odds ratio 4.79, 95% confidence interval 1.44-15.9) and dyslipidemia (odds ratio 11.6, 95% confidence interval 5.65-23.9) increased risk for possible NAFLD but not income:poverty ratio, hours spent on computer use, or added sugars. Although HBV prevalence has decreased in recent years among US children and adolescents, HCV and possible NAFLD have increased. Public health efforts must seek further understanding of the driving factors of this increase so that age-appropriate interventions can be developed and implemented.

Objective: To evaluate the association between non-alcoholic fatty liver disease (NAFLD), heart failure (HF), and all-cause mortality. Background: Both NAFLD and HF are increasing in prevalence due to shared risk factors. Methods: We used data from the National Health and Nutrition Examination Survey (NHANES) 2005-2018 to identify non-pregnant individuals aged ≥20 years with HF and NAFLD and linked with the cause of death data from the National Center for Health Statistics. The associations between NAFLD, HF, and all-cause mortality were assessed using logistic regression and Cox proportional hazard modeling as appropriate. Results: There were 82,358,893 weighted eligible participants of whom 3,833,667 (4.7%) had NAFLD. The mean (SE) age was 51.5 (0.35) years, 45.1% women, 63.0% Non-Hispanic White and 11.8% Non-Hispanic Black. Cardiovascular comorbidities were more common in participants with NAFLD; they were more likely to have hypertension (81.7% vs 53.5%), diabetes (65.1% vs 17.1%), stroke (7.3% vs 4.1%), coronary artery disease (14.9% vs 8.4%), or HF (10.5% v s 3.5%) compared with participants without NAFLD. In multivariate logistic regression models adjusting for age, race/ethnicity and sex, participants with NAFLD were 3.5 times more likely to have HF [aOR, 95% CI: 3.47 (1.98-6.06)]. Older age, male sex, presence of diabetes and coronary artery disease were associated with higher odds of HF in participants with established NAFLD. At the end of the follow-up period, participants with NAFLD had higher all-cause mortality compared with participants without NAFLD [HR(95% CI): 1.93 (1.24-2.99), p&lt;0.001]. Conclusion: In this analysis of US adults, ambulatory participants with NAFLD were ~3.5 times more likely to have HF, and twice as likely to experience mortality compared with participants without NAFLD. Further studies are needed to identify the possible linkage between NAFLD and HF beyond the shared risk factor pathogenesis.

Non-Alcoholic Fatty Liver Disease, Heart Failure, and Long-Term Mortality: Insights From the National Health and Nutrition Examination Survey

These recommendations are based on the following: (1) a formal review and analysis of the recently published world literature on the topic [Medline search up to June 2011]; (2) the American College of Physicians’ Manual for Assessing Health Practices and Designing Practice Guidelines; (3) guideline policies of the three societies approving this document; and (4) the experience of the authors and independent reviewers with regards to NAFLD. Intended for use by physicians and allied health professionals, these recommendations suggest preferred approaches to the diagnostic, therapeutic and preventive aspects of care. They are intended to be flexible and adjustable for individual patients. Specific recommendations are evidence-based wherever possible, and when such evidence is not available or inconsistent, recommendations are made based on the consensus opinion of the authors. To best characterize the evidence cited in support of the recommendations, the AASLD Practice Guidelines Committee has adopted the classification used by the Grading of Recommendation Assessment, Development, and Evaluation (GRADE) workgroup with minor modifications (Table 1). The strength of recommendations in the GRADE system is classified as strong (1) or weak (2). The quality of evidence supporting strong or weak recommendations is designated by one of three levels: high (A), moderate (B) or low-quality (C). This is a practice guideline for clinicians rather than a review article and interested readers can refer to several comprehensive reviews published recently.

A meta-analysis of 10 prospective cohort studies,1 including our own,2 reported that serum γ-glutamyltransferase (GGT) predicted incident vascular events. This meta-analysis posed one important, but unsolved question: why does serum GGT predict incident vascular events? In addition to vascular events, serum GGT predicts various important clinical outcomes including type 2 diabetes, metabolic syndrome, and renal problems.3–5 Serum GGT has traditionally been used as a marker of alcohol consumption; however, alcohol consumption cannot explain the disease relationships with serum GGT because these associations have been observed among nondrinkers as well as drinkers. The other prevailing interpretations are that serum GGT predicts clinical outcomes as a marker of nonalcoholic fatty liver disease (NAFLD) or oxidative stress.6–8 Although both of these explanations have some merit, each also has problems. Although not clearly stated in many of the reports,1–5 most associations of serum GGT with clinical outcomes were dose-response relations within the normal range of serum GGT; we submit that this aspect of the association is critical to interpretation. First, even though NAFLD may partially explain the associations among subjects with a relatively high serum GGT activity and NAFLD can present even among subjects with low normal serum GGT, NAFLD is unlikely to fully explain the graded associations with clinical outcomes which were observed among subjects with serum GGT in the low part of its normal range, less than 20 or 30 U/L. However, it is worthwhile to note that serum GGT may be a predictor of the future risk of NAFLD. In a prospective study by our group,9 serum GGT within its normal range strongly predicted the future risk of chronic elevation of serum alanine aminotransferase (ALT), but serum ALT within its normal range did not predict the future risk of chronic elevation of serum GGT. The …

Background and Aims: Nonalcoholic fatty liver disease (NAFLD) is a global health problem, and dietary intervention is still considered one of the primary interventions. This study aimed to examine cross-sectional associations between dietary and serum levels of folate and NAFLD. Methods: We conducted a study of 7543 adults who participated in the National Health and Nutrition Examination Survey, 2009-2018. NAFLD status was determined by a fatty liver index (FLI) value ≥60. Multivariable logistic regression models were used to estimate associations between folate and NAFLD. Results: Almost half (45%) of the patients were classified as having NAFLD based on the FLI. In the fully adjusted model, participants in the highest quartile of dietary total folate and food folate were found to have a lower prevalence of NAFLD than those in the lowest quartile [odds ratio (OR)quartile 4 versus 1 = 0.582; 95% confidence interval (CI) = 0.350-0.968; and ORquartile 4 versus 1 = 0.737; 95% CI = 0.611-0.888, respectively], and the fourth quartile values of serum total folate and 5-methyl-tetrahydrofolate were significantly negatively associated with NAFLD prevalence (ORquartile 4 versus 1 = 0.664; 95% CI = 0.495-0.891; and ORquartile 4 versus 1 = 0.712; 95% CI = 0.532-0.954, respectively). Subgroup analyses revealed that this beneficial association was more significant in women (ORquartile 4 versus 1 = 0.526; 95% CI = 0.329-0.843; pinteraction < 0.001) than in men (ORquartile 4 versus 1 = 0.805; 95% CI = 0.546-1.186). Conclusions: Higher dietary folate intake and serum folate levels are associated with a lower NAFLD prevalence among U.S. adults and the trend is more pronounced among women, indicating opportunities for dietary NAFLD interventions.

BackgroundIron metabolism may be involved in the pathogenesis of the non-alcoholic fatty liver disease (NAFLD). The relationship between iron metabolism and NAFLD has not been clearly established. This study aimed to clarify the relationship between biomarkers of iron metabolism and NAFLD.MethodsBased on the National Health and Nutrition Examination Survey (NHANES), restricted cubic spline models and multivariable logistic regression were used to examine the association between iron metabolism [serum iron (SI), serum ferritin (SF), transferrin saturation (TSAT), and soluble transferrin receptor (sTfR)] and the risk for NAFLD. In addition, stratified subgroup analysis was performed for the association between TSAT and NAFLD. Moreover, serum TSAT levels were determined in male mice with NAFLD. The expression of hepcidin and ferroportin, vital regulators of iron metabolism, were analyzed in the livers of mice by quantitative real-time PCR (qRT-PCR) and patients with NAFLD by microarray collected from the GEO data repository.ResultsPatients with NAFLD showed decreased SI, SF, and TSAT levels and increased STfR levels based on the NHANES. After adjusting for confounding factors, TSAT was significantly negatively correlated with NAFLD. Of note, the relationship between TSAT and NAFLD differed in the four subgroups of age, sex, race, and BMI (P for interaction < 0.05). Consistently, mice with NAFLD exhibited decreased serum TSAT levels. Decreased hepcidin and increased ferroportin gene expression were observed in the livers of patients and mice with NAFLD.ConclusionSerum TSAT levels and hepatic hepcidin expression were decreased in both patients and mice with NAFLD. Among multiple biomarkers of iron metabolism, lower TSAT levels were significantly associated with a higher risk of NAFLD in the U.S. general population. These findings might provide new ideas for the prediction, diagnosis, and mechanistic exploration of NAFLD.