Patients with non-alcoholic fatty liver disease may benefit from increased dietary niacin intake

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A recent large-scale prospective cohort study published JAMA Network Open, Researchers evaluated whether higher dietary niacin intake reduced the risk of all-cause, heart, and cerebrovascular disease(s)-related mortality in adults with nonalcoholic fatty liver disease (NAFLD) in the United States (US).

Study: Dietary Niacin Intake and Mortality in People with Alcoholic Fatty Liver Disease.  Image credit: monticello/Shutterstock.comStudy: Dietary niacin intake and mortality in individuals with nonalcoholic fatty liver disease. Image credit: monticello/


The burden of NAFLD is increasing worldwide, with the estimated prevalence of the disease reaching 32.4% worldwide and 47.8% in the United States. Even the global NAFLD mortality rate has doubled in the last three decades.

Existing evidence indicates that cardiovascular disease (CVD) is the primary cause of death in patients with NAFLD.

However, no prospective studies have evaluated the association between nutritional, specifically, niacin intake and mortality risk in NAFLD patients.

A previous animal study showed that niacin supplementation increased nicotinamide adenine dinucleotide (NAD) levels that help regenerate a fatty liver, and a study with human subjects showed how it improved muscle performance.

Niacin, or vitamin B3, is a precursor for the synthesis of NAD and nicotinamide adenine dinucleotide phosphate (NADP), two pyridine coenzymes that play essential roles in various metabolic, energy metabolism and redox reactions.

Preclinical studies have also shown that niacin inhibits or reverses inflammation and hepatic steatosis to prevent fibrosis.

About the study

In the current study, researchers used data from 20-year-old US adults who participated in eight cycles of the National Health and Nutrition Examination Survey (NHANES) spanning 2003 to 2018.

They classified individuals aged ≤39, 40–59 and ≥60 into three groups.

They self-report data on hypertension, dyslipidemia and diabetes. Other study covariates were race/ethnicity, educational status, income, body mass index (BMI), use of dietary supplements, physical activity, and smoking status.

The team ascertained mortality by linking NHANES data to National Death Index records through December 31, 2019.

Similarly, they measured dietary niacin intake using a standardized automated multiple-pass method (AMPM), which involved two 24-hour dietary recall interviews, one in person and the other by telephone, to collect data on intake type and food quantity. by each participant.

They calculated their daily dietary niacin intake based on the average of the participants’ two diet recalls.

Statistical analysis in these studies included unweighted frequencies and weighted percentages for categorical variables, while they used medians and IQRs for continuous variables.

The researchers used weighted Cox proportional hazards models to assess the association between dietary niacin intake and all-cause mortality and CVD mortality, presenting results as hazard ratios (HRs) and 95% confidence intervals (CIs).

In addition, they used restricted cubic spline analysis to investigate nonlinear associations between dietary niacin intake and mortality, further stratifying them to assess interactions with different factors.


In all, 80,312 people participated in NHANES from 2003 to 2018, of whom 6,540 had a fatty liver index (FLI) ≥30; However, of these, only 4,315 have confirmed NAFLD and the majority are men.

Baseline characteristics of study participants varied based on dietary niacin intake; For example, those with higher niacin in their diets were younger and more often male.

The authors noted an association of higher dietary niacin intake (≥26.7 mg/d) with a 30% lower risk and ~50% lower risk of CVD-related mortality in patients with NAFLD.

The latter association became insignificant after adjusting for potential confounding variables other than age and gender.

Furthermore, evidence of a nonlinear association between dietary niacin intake and these two types of mortality was lacking.

In subgroup analyses, the association of higher niacin intake with mortality risk was stronger only for NAFLD patients without diabetes compared to the reference group.

Compared to the reference group, the subgroups with and without diabetes had HRs of 0.82 and 0.58 for all-cause mortality, respectively. p= 0.04 for the interaction.

In the subgroup of adults with vitamin B6 intake <1.7 mg, the all-cause mortality was 0.26, indicating that they may benefit more from dietary niacin intake. Notably, vitamin B6 is essential for the biosynthesis of niacin and its metabolism.

A daily niacin dose of at least 20 mg also meets the requirement for NAD+ synthesis, any dysregulation of which is associated with CVD, obesity and neurodegenerative diseases.

Stratified and sensitivity analyzes further demonstrated the robustness of these findings.


Overall, the results of the current study conducted in NAFLD patients suggest an association between higher dietary niacin intake and reduced all-cause mortality.

However, there was no inverse association between dietary niacin intake and risk of CVD mortality.

Future studies should investigate the dose-response relationship of dietary niacin intake with mortality to determine its optimal dose for patients with NAFLD.

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