Research Article | | Peer-Reviewed

Plant-Based Retinol Intake and Risk of Nonalcoholic Fatty Liver Disease in American Adults: Insights from NHANES 2007-2014

Received: 18 July 2025     Accepted: 29 August 2025     Published: 5 September 2025
Views:       Downloads:
Abstract

Existing evidence suggests a strong correlation between nonalcoholic fatty liver disease (NAFLD) risk and dietary factors, and this investigation aimed to examine the association between dietary factors and NAFLD risk in American adults. Utilizing data from the National Health and Nutrition Examination Survey (NHANES) conducted between 2007 and 2014, the study employed chi-square tests of independence and t-tests to analyze differences between the NAFLD and control groups, while logistic regression analysis was used to identify factors influencing NAFLD risk and assess the association of plant-based dietary retinol intake with such risk. The NAFLD group consisted of 1,286 males (53.5%) and 1,138 females (46.9%), and logistic regression analysis identified uric acid (UA), high-density lipoprotein (HDL), smoking, vigorous recreational activity, hypertension, diabetes, gender, BMI, race, annual household income, and plant-based retinol intake as significant predictors of NAFLD (P < 0.05), with notably higher dietary intake of plant-based retinol being associated with a lower risk of NAFLD (OR = 0.670, 95% CI: 0.532-0.842). This study demonstrates that specific dietary components, especially plant-based retinol, play an important role in influencing NAFLD risk among American adults, and further long-term research is needed to inform public health initiatives aimed at reducing NAFLD prevalence.

Published in World Journal of Public Health (Volume 10, Issue 3)
DOI 10.11648/j.wjph.20251003.29
Page(s) 379-388
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2025. Published by Science Publishing Group

Keywords

NAFLD, Dietary Factor, Plant-based Retinol, Logistic Regression Model, NHANES

1. Introduction
Nonalcoholic fatty liver disease (NAFLD) is a disease process and a set of symptoms that are distinguished by the deposition of fat in the liver. Individual who consumes excessive amounts of alcohol or suffers from other liver disorders are not affected by this disease . Liver damage progresses through a series of stages, commencing with simple hepatic steatosis and progressing to nonalcoholic steatohepatitis (NASH), liver fibrosis, cirrhosis, and ultimately hepatocellular carcinoma (HCC) . In recent years, there has been a significant rise in the global prevalence of NAFLD, estimates indicate that 10% to 35% of the population is affected by NAFLD . Nearly 30% of adults in the United States are affected by this condition . Research suggests that NAFLD is associated with an increased risk of chronic diseases, including cardiovascular disease, obesity, diabetes, and hypertension .
Epidemiological studies have shown a correlation between dietary factors and the prevalence of nonalcoholic fatty liver disease (NAFLD) . Studies have shown a positive correlation between the consumption of refined grains, fried foods, processed meats, and fructose-rich foods and an elevated risk of NAFLD . On the other hand, a diet rich in fruits, vegetables, legumes, probiotic dairy products, and whole grains is believed to lower the risk of developing NAFLD . Furthermore, studies have shown that the intake of vitamin A (retinol), known for its antioxidant properties, significantly influences the prevalence of NAFLD . Researchers have conducted research to investigate the potential correlation between dietary retinol and non-alcoholic fatty liver disease (NAFLD). Despite examining a potential association between dietary retinol and NAFLD, the research yielded conflicting results due to differences in ethnic background, dietary habits, study design, and sample sizes. Higher intakes of retinol were associated with a reduced risk of developing NAFLD in an Iranian study . In an additional cross-sectional study that involved 80 individuals, individuals with NAFLD consumed a greater amount of vitamin A than healthy controls . Consequently, it is crucial to investigate the risk of NAFLD in addition to dietary factors. This cross-sectional study employed a logistic regression model to examine the factors that influence NAFLD risk, thereby improving the administration of adult health.
2. Materials and Methods
2.1. The Subjects and Data Collection
Figure 1. Flowchart of individual selection.
This cross-sectional study used data from four consecutive two-year cycles (2007-2014) of the National Health and Nutrition Examination Survey (NHANES). The survey utilized a multistage, stratified sampling design to obtain a representative sample of the noninstitutionalized civilian population of the United States . Data collection involved conducting household interviews with participants along with medical examinations to obtain blood and urine samples. We collected specimens during household visits for participants unable to attend medical examinations due to health limitations . The NHANES dataset initially included 40,617 participants (20,180 males and 20,437 females), with the analysis focused on 23,482 individuals aged 20 years or older. We conducted subsequent analyses on 9,754 participants, excluding those with the United States Fatty Liver Index (USFLI; n = 13,728). Additionally, the study excluded 200 participants who tested positive for hepatitis B surface antigen or hepatitis C virus antibodies. The study also excluded participants who consumed alcohol at a rate of less than 10 g/day for women and less than 20 g/day for men (n = 1,535). People who were pregnant (n = 94), had unreliable or incomplete dietary recall data (n = 1,224), were missing weight data (n = 8), or had an average energy intake that was more than or less than three standard deviations from the mean (n = 80) were also not included (Figure 1). Ultimately, the final analysis included 6,613 participants (3,067 males and 3,546 females). The Research Ethics Review Board of the National Center for Health Statistics approved the study protocol, and all participants provided written informed consent.
2.2. NAFLD Measurement
The United States Fatty Liver Index (USFLI), with a cutoff value of 30, assessed NAFLD based on age, race, waist circumference, fasting glucose, gamma-glutamyl transferase, and fasting insulin . As previously reported, the USFLI is a reliable, noninvasive measure of NAFLD and serves as an independent predictor of liver-related and all-cause mortality .
2.3. Dietary Retinol Intake
Dietary vitamin A intake, primarily through retinol, was quantified using two 24-hour dietary recall interviews to calculate retinol activity equivalents (mcg) . We conducted the initial recall at the mobile examination center and conducted the second recall by telephone 3 to 10 days later. We used the average retinol intake from the two recalls for analysis. Detailed methodologies of the dietary recall interviews are available in previous publications . Based on specific food codes, we identified the sources of dietary retinol intake, which included animal-derived sources like meat, eggs, dairy products, poultry, and fish, as well as plant-based sources like legumes, nuts, seeds, fruits, and vegetables. We quantified the animal-derived retinol intake using the conversion factor of 1 mcg retinol activity equivalents (RAE), which corresponds to 1 mcg of all-trans retinol from animal-based foods. We estimated plant-based retinol using the following equation: 1 RAE (mcg) = 1/12 beta-carotene (mcg) + 1/24 other provitamin A (mcg).
2.4. Covariates
Researchers have used the food frequency questionnaire, known for its validity and reliability, to assess average dietary intakes , which include those from milk and milk products, meat, poultry, fish, mixed dishes, eggs, legumes, nuts, seeds, grain products, fruits, and vegetables. Multiple potential factors were assessed, which includes gender (male and female), age groups (20-44 years, 45-59 years, 60-74 years, and ≥75 years), race/ethnicity (Mexican-Americans, other Hispanics, non-Hispanic Whites, non-Hispanic Blacks, and other races), body mass index (BMI) categories (normal: <25 kg/m²; overweight: 25 to <30 kg/m²; obese: ≥30 kg/m²), educational level (less than high school, high school, and post-high school), annual household income (<$20,000, $20,000-$44,999, $45,000-$74,999, and ≥$75,000), smoking history (ever smoked at least 100 cigarettes or never), participation in vigorous recreational activity (yes or no), diabetes status (yes or no), hypertension status (yes or no), and biochemical parameters including low-density lipoprotein (LDL), high-density lipoprotein (HDL), total cholesterol (TC), and uric acid (UA). Additionally evaluated the mean energy consumption, overall dietary retinol intake, retinol intake from animal sources, and retinol intake from plant sources. Diabetes is shown by fasting blood glucose levels of ≥7.0 mmol/L and 2-hour plasma glucose levels of ≥11.1 mmol/L, using diabetes medicines or insulin, or saying that a doctor told you that you have diabetes . Hypertension is characterized by a mean systolic blood pressure of ≥130 mmHg and/or a mean diastolic blood pressure of ≥80 mmHg, the utilization of antihypertensive medication, or self-reported physician-diagnosed hypertension .
2.5. Statistical Analysis
We used the student’s t-test to evaluate inter-group differences for continuous variables and the chi-square test for categorical data. Categorical variables were depicted as percentage frequencies, while continuous data were presented as mean values (standard deviation [SD]). The factors that influence NAFLD were investigated using logistic regression analysis, which yielded odds ratios (ORs) and 95% confidence intervals (CIs). Multivariable-adjusted logistic regression model was utilized to assess the relationship between plant-based dietary retinol intake and NAFLD risk. Some potential confounders included gender, age, race, education level, smoking status, physical activity, income level, BMI, hypertension, diabetes, TC and UA. Stata 15.0 was employed to conduct statistical analyses, ensuring that the sample weights and units were appropriate for national representativeness. A 2-tailed p-value of less than 0.05 was used to determine the statistical significance of all tests.
3. Results
3.1. Description of the Participants
Table 1 shows that 1286 males (53.55%) and 1138 females (44.95%) received a diagnosis of NAFLD. We found that the participants with NAFLD and the healthy controls exhibited statistically significant differences in the presence of influencing factors, including gender, age, race, BMI, education level, annual household income, smoking status, vigorous recreational activity, hypertension, diabetes, UA, HDL, animal-derived dietary retinol, and plant-based dietary retinol (P < 0.05).
3.2. Influencing Factors of NAFLD Risk
The characteristics that influence the risk of NAFLD as identified using logistic regression analysis (Table 2). Male gender compared to female had significant positive associations with NAFLD risk (OR = 1.694, 95% CI: 1.139-1.374), BMI (OR = 4.891, 95% CI: 4.410-5.425), smoking compared to non-smoking (OR = 1.305, 95% CI: 1.138-1.497), hypertension versus non-hypertension (OR = 1.531, 95% CI: 1.316-1.779), diabetes compared to non-diabetes (OR = 2.648, 95% CI: 2.250-3.118), and UA levels (OR = 1.360, 95% CI: 1.288-1.436). Conversely, we observed significant negative associations with NAFLD risk for factors such as race (OR = 0.608, 95% CI: 0.571-0.647), annual household income (OR = 0.908, 95% CI: 0.851-0.968), vigorous recreational activity (OR = 0.599, 95% CI: 0.495-0.726), HDL levels (OR = 0.958, 95% CI: 0.952-0.963), and plant-based dietary retinol intake (OR = 0.886, 95% CI: 0.847-0.926).
3.3. Association Between Plant-based Dietary Retinol Intake and NAFLD Risk
The association of plant-based dietary retinol intake with the risk of NAFLD was indicated according to multivariable-adjusted logistic regression model (Table 3, Figure 2). There was significantly negative relationship between plant-based dietary retinol intake and the risk of NAFLD (OR: 0.637, 95% CI: 0.515-0.788). This association remained significant after adjusting some potential confounders (OR: 0.670, 95% CI: 0.532-0.842).
Table 1. Characteristics of the study individuals based on NAFLD.

Group

NAFLD (total)a

p-valueb

no

yes

Gender (n, %)

<0.001

Male

1781 (42.52%)

1286 (53.05%)

Female

2408 (57.48%)

1138 (46.95%)

Age Group (n, %)

<0.001

20-44 years

1890 (45.12%)

709 (29.25%)

45-59 years

988 (23.59%)

655 (27.02%)

60-74 years

862 (20.58%)

742 (30.61%)

≥75 years

449 (10.72%)

318 (13.12%)

Race/Ethnicity (n, %)

<0.001

Mexican American

488 (11.65%)

552 (22.77%)

Other Hispanic

444 (10.60%)

294 (12.13%)

Non-Hispanic White

1845 (44.04%)

1155 (47.65%)

Non-Hispanic Black

931 (22.22%)

269 (11.10%)

Other/Multiracial

481 (11.48%)

154 (6.35%)

BMI (n, %)

<0.001

<25 kg/m2

1716 (41.02%)

108 (4.46%)

25 to <30 kg/m2

1568 (37.49%)

637 (26.32%)

≥30 kg/m2

899 (21.49%)

1675 (69.21%)

Educational Level (n, %)

<0.001

< High school

902 (21.55%)

802 (33.14%)

High school

954 (22.80%)

543 (22.44%)

> High school

2329 (55.65%)

1075 (44.42%)

Annual household income (n, %)

<0.001

<$20,000

780 (19.45%)

561 (24.14%)

$20,000-$44,999

1352 (33.71%)

931 (40.06%)

$45,000-$74,999

781 (19.47%)

409 (17.60%)

≥$75,000

1098 (27.37%)

423 (18.20%)

Smoking status (n, %)

<0.001

Yes

1576 (37.64%)

1131 (46.66%)

No

2611 (62.36%)

1293 (53.34%)

Vigorous recreational activity (n, %)

<0.001

Yes

1031 (24.61%)

270 (11.14%)

No

3158 (75.39%)

2154 (88.86%)

Hypertension (n, %)

<0.001

Yes

1648 (39.34%)

1539 (63.49%)

No

2541 (60.66%)

885 (36.51%)

Diabetes (n, %)

<0.001

Yes

505 (12.06%)

910 (37.54%)

No

3684 (87.94%)

1514 (62.46%)

Cholesterol: mean (SD), mg/dL

192.16 (41.19)

194.23 (41.79)

0.051

Uric Acid: mean (SD), mg/dL

5.14 (1.30)

6.03 (1.43)

<0.001

HDL: mean (SD), mg/dL c

56.28 (14.86)

45.78 (11.87)

<0.001

LDL: mean (SD), mg/dL d

114.86 (35.13)

115.34 (35.95)

0.605

Average energy intake: mean (SD), kcal/day

1903.27 (695.88)

1912.03 (711.51)

0.625

Total dietary retinol intake: mean (SD), μg/1000kcal/day

338.66 (284.09)

325.69 (279.77)

0.072

Animal-derived dietary retinol intake: mean (SD), μg/1000kcal/day)

122.70 (150.62)

134.97 (205.69)

0.005

Plant-based dietary retinol intake: mean (SD), μg/1000kcal/day)

198.80 (238.80)

171.24 (181.11)

<0.001

a Data are presented as No. (%) of participants, unless otherwise noted. Percentages have been rounded and may not add up to 100.
b The means of continuous variables were compared using independent 2-sample t tests. The distribution of categorical variables was compared using Pearson χ2 tests.
c HDL, high-density lipoprotein.
d LDL, low density lipoprotein.
Table 2. Multivariate logistic regression analysis on relating factors of NAFLD.

Variable

B

SE

Wald χ2

P

OR (95%CI)

Gender

0.517

0.077

47.144

<0.001

1.694 (1.139,1.374)

BMI

1.587

0.053

902.079

<0.001

4.891 (4.410,5.425)

Race/Ethnicity

-0.498

0.032

239.729

<0.001

0.608 (0.571,0.647)

Annual household income

-0.097

0.033

8.662

0.003

0.908 (0.851,0.968)

Smoking

0.266

0.070

14.481

<0.001

1.305 (1.138,1.497)

Vigorous recreational activity

-0.512

0.098

27.334

0.001

0.599 (0.495,0.726)

Hypertension

0.426

0.077

30.652

<0.001

1.531 (1.316,1.779)

Diabetes

0.974

0.083

136.784

<0.001

2.648 (2.250,3.118)

Uric Acid

0.308

0.028

122.992

<0.001

1.360 (1.288,1.436)

HDL

-0.043

0.003

197.819

<0.001

0.958 (0.952,0.963)

Plant-based dietary retinol intake

-0.121

0.023

28.106

<0.001

0.886 (0.847,0.926)

SE, standard error; OR, odds ratio; CI, confidence interval.
Table 3. Association between plant-based dietary retinol intake and NAFLD risk.

Variables

Model1a

Mode2b

Mode3c

OR (95%CI)

P value

OR (95%CI)

P value

OR (95%CI)

P value

Plant-based dietary retinol intake (RAEs, μg/1000kcal/day)

<70.37

1.00 (ref.)

1.00 (ref.)

1.00 (ref.)

70.37 to <138.53

0.949 (0.781-1.152)

0.589

0.943 (0.766-1.160)

0.574

1.015 (0.820-1.258)

0.886

138.53 to <253.07

0.855 (0.704-1.038)

0.111

0.821 (0.668-1.010)

0.062

0.899 (0.710-1.138)

0.367

≥253.07

0.637 (0.515-0.788)

<0.001

0.588 (0.465-0.745)

<0.001

0.670 (0.532-0.842)

0.001

a Crude model.
b The model included covariates (i.e. gender and age).
c The model included covariates (i.e. gender, age, race, education level, smoking status, physical activity, income level, BMI, hypertension, diabetes, TC and UA).
Figure 2. Association between plant-based dietary retinol intake and NAFLD risk. Hazard ratios and 95% confidence intervals (error bars) were calculated using covariate-adjusted method. Covariates were as follows: gender, age, race, education level, smoking status, physical activity, income level, BMI, hypertension, diabetes, TC and UA.
4. Discussion
The application of logistic regression models is of considerable significance in the field of public health research. By utilizing dietary factors to identify populations at a high risk of NAFLD, these models provide a valuable preliminary screening tool that informs targeted prevention strategies. Noninvasive methods can readily access and evaluate the variables employed in this model . Additionally, the model's generalizability to the general population is further enhanced by its ability to be implemented through computer programs, which enables the automated calculation of NAFLD risk probabilities based on the factors that are included. However, additional research is necessary to ascertain the relevance of these risk estimates to individuals.
Our results suggest that dietary factors significantly influence the risk of NAFLD. It is important to note that the intake of dietary retinol from plants was associated with lower odds of NAFLD. Despite the uncertainty surrounding the precise mechanisms underlying this relationship, numerous potential explanations have emerged. This effect may be influenced by the abundance of provitamin A carotenoids in plant-based diets. Our study estimated the intake of plant-based retinol by analyzing the consumption of foods such as legumes, beans, fruits, and vegetables. Research indicates that the antioxidant properties of carotenoids may mitigate oxidative stress in hepatocytes, thereby reducing the risk of NAFLD and protecting against liver injury . A lot of research has also shown that high-sensitivity C-reactive protein (hs-CRP) and the inflammatory cytokines IL-6 and TNF-α are linked to NAFLD and may be biomarkers of inflammation that lead to endothelial cell injury . Iwaki et al. also reported that vitamin A and its metabolites may either directly or indirectly regulate the expression of adiponectin. It is possible that adiponectin's anti-inflammatory properties could lower the risk of NAFLD by blocking the expression of nuclear factor-kappa B (NF-κB) and TNF-α, which fights inflammation . Furthermore, vitamin A provides an additional protective mechanism by regulating hepatic glucose and lipid metabolism .
The progression of NAFLD is considerably influenced by lifestyle factors, including dietary choices and demographic characteristics, as evidenced by a variety of studies . For instance, prior research has shown that individuals with NAFLD are more likely to consume diets that are high in energy, total fat, saturated fat, and fructose, while they are lower in fiber and polyunsaturated fatty acids (PUFAs) than healthy individuals . Additionally, research indicates that obesity is a significant risk factor for NAFLD, with its prevalence increasing as BMI increases . A six-year study in China found that individuals with NAFLD had a greater risk of developing diabetes than healthy controls . Smoking was identified as an independent risk factor for the onset and progression of NAFLD in our research . This may be because of nicotine on the sympathetic nervous system, which increases the secretion of glucagon and catecholamines, thereby fostering the development of NAFLD .
There are numerous noteworthy advantages to our investigation. Initially, the use of a nationally representative sample of adults in the United States improved the statistical power and generalizability of our findings. Secondly, the study employed a logistic regression model that included dietary factors to assess the risk of NAFLD, thereby illustrating its potential for use in health management and NAFLD prevention initiatives among American adults.
Nevertheless, this investigation is subject to certain inherent limitations. Initially, the cross-sectional design obstructs the establishment of a causal relationship between dietary factors and NAFLD. Secondly, the use of two 24-hour dietary recall datasets may introduce recall bias. Third, we used a previously validated index instead of a clinical diagnosis to determine NAFLD status. We have effectively developed a highly accurate risk prediction model to assess the combined impact of individual dietary factors on NAFLD, despite these limitations.
5. Conclusions
In conclusion, this study demonstrated an inverse association between plant-based dietary retinol intake and NAFLD risk in a national adult population in America. The findings revealed that individual diet information could be applied to explore the risk of NAFLD in American adults. Further prospective studies are required to improve the health lever of human.
Abbreviations

NAFLD

Nonalcoholic Fatty Liver Disease

NHANES

National Health and Nutrition Examination Survey

HDL

High-density Lipoprotein

UA

Uric Acid

BMI

Body Mass Index

NASH

Nonalcoholic Steatohepatitis

HCC

Hepatocellular Carcinoma

USFLI

United States Fatty Liver Index

RAE

Retinol Activity Equivalents

LDL

Low-density Lipoprotein

TC

Total Cholesterol

SD

Standard Deviation

ORs

Odds Ratios

CIs

Confidence Intervals

hs-CRP

High-sensitivity C-reactive Protein

NF-κB

Nuclear Factor-kappa B

PUFAs

Polyunsaturated Fatty Acids

Acknowledgments
The authors thank all of the people who participated in this study.
Ethics Approval and Consent to Participate
Not applicable.
Consent for Publication
Not applicable.
Availability of Data and Materials
The datasets generated for this study is available in online repositories. The repository/repositories name and accession number(s) can be found below: https://www.cdc.gov/nchs/nhanes/index.htm.
Conflicts of Interest
The authors declare that they have no competing interests.
References
[1] Angulo P. Nonalcoholic fatty liver disease. N Engl J Med. 2002; 346: 1221-31.
[2] Vadarlis A, Antza C, Bakaloudi DR, Doundoulakis I, Kalopitas G, Samara M, Dardavessis T, Maris T, Chourdakis M. Systematic review with meta-analysis: The effect of vitamin E supplementation in adult patients with non-alcoholic fatty liver disease. J Gastroenterol Hepatol. 2021; 36: 311-9.
[3] Afzali N, Ebadi SS, Afzali H, Sharif MR, Vazirian M, Ebadi SA, Shahkarami V, Rahimi H. Effect of beta vulgaris extract on liver enzymes in patients with non-alcoholic fatty liver disease: A randomized clinical trial. Hepat Mon. 2020; 20: e102125.
[4] Younossi Z, Anstee QM, Marietti M, Hardy T, Henry L, Eslam M, George J, Bugianesi E. Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention. Nat Rev Gastroenterol Hepatol. 2018; 15: 11-20.
[5] Estes C, Razavi H, Loomba R, Younossi Z, Sanyal AJ. Modeling the epidemic of nonalcoholic fatty liver disease demonstrates an exponential increase in burden of disease. Hepatology. 2018; 67: 123-33.
[6] Lotfi A, Saneei P, Hekmatdost A, Salehisahlabadi A, Shiranian A, Ghiasvand R. The relationship between dietary antioxidant intake and physical activity rate with nonalcoholic fatty liver disease (NAFLD): A case - Control study. Clin Nutr ESPEN. 2019; 34: 45-9.
[7] Le MH, Devaki P, Ha NB, Jun DW, Te HS, Cheung RC, Nguyen MH. Prevalence of non-alcoholic fatty liver disease and risk factors for advanced fibrosis and mortality in the United States. PLoS One. 2017; 12: e0173499.
[8] Li H, Gu Y, Wu X, Rayamajhi S, Bian S, Zhang Q, Meng G, Liu L, Wu H, Zhang S, et al. Association between consumption of edible seaweeds and newly diagnosed non-alcohol fatty liver disease: The TCLSIH Cohort Study. Liver Int. 2021; 41: 311-20.
[9] Younossi ZM, Henry L. The impact of obesity and type 2 diabetes on chronic liver disease. Am J Gastroenterol. 2019; 114: 1714-5.
[10] Targher G, Byrne CD, Lonardo A, Zoppini G, Barbui C. Non-alcoholic fatty liver disease and risk of incident cardiovascular disease: A meta-analysis. J Hepatol. 2016; 65: 589-600.
[11] Vahid F, Hekmatdoost A, Mirmajidi S, Doaei S, Rahmani D, Faghfoori Z. Association between index of nutritional quality and nonalcoholic fatty liver disease: The role of vitamin D and B group. Am J Med Sci. 2019; 358: 212-8.
[12] Aktary ML, Eller LK, Nicolucci AC, Reimer RA. Cross-sectional analysis of the health profile and dietary intake of a sample of Canadian adults diagnosed with non-alcoholic fatty liver disease. Food Nutr Res. 2020; 64: 4548.
[13] Mollard RC, Sénéchal M, MacIntosh AC, Hay J, Wicklow BA, Wittmeier KD, Sellers EA, Dean HJ, Ryner L, Berard L, McGavock JM. Dietary determinants of hepatic steatosis and visceral adiposity in overweight and obese youth at risk of type 2 diabetes. Am J Clin Nutr. 2014; 99: 804-12.
[14] Ouyang X, Cirillo P, Sautin Y, McCall S, Bruchette JL, Diehl AM, Johnson RJ, Abdelmalek MF. Fructose consumption as a risk factor for non-alcoholic fatty liver disease. J Hepatol. 2008; 48: 993-9.
[15] Shim P, Choi D, Park Y. Association of blood fatty acid composition and dietary pattern with the risk of non-alcoholic fatty liver disease in patients who underwent cholecystectomy. Ann Nutr Metab. 2017; 70: 303-11.
[16] Dorosti M, Jafary Heidarloo A, Bakhshimoghaddam F, Alizadeh M. Whole-grain consumption and its effects on hepatic steatosis and liver enzymes in patients with non-alcoholic fatty liver disease: a randomised controlled clinical trial. Br J Nutr. 2020; 123: 328-36.
[17] Koutnikova H, Genser B, Monteiro-Sepulveda M, Faurie JM, Rizkalla S, Schrezenmeir J, Clément K. Impact of bacterial probiotics on obesity, diabetes and non-alcoholic fatty liver disease related variables: a systematic review and meta-analysis of randomised controlled trials. BMJ Open. 2019; 9: e017995.
[18] Maleki Z, Jazayeri S, Eslami O, Shidfar F, Hosseini AF, Agah S, Norouzi H. Effect of soy milk consumption on glycemic status, blood pressure, fibrinogen and malondialdehyde in patients with non-alcoholic fatty liver disease: a randomized controlled trial. Complement Ther Med. 2019; 44: 44-50.
[19] Al-Busafi SA, Bhat M, Wong P, Ghali P, Deschenes M. Antioxidant therapy in nonalcoholic steatohepatitis. Hepat Res Treat. 2012; 2012: 947575.
[20] Chen G. The link between hepatic vitamin a metabolism and nonalcoholic fatty liver disease. Curr Drug Targets. 2015; 16: 1281-92.
[21] Lim HS, Choi J, Lee B, Kim SG, Kim YS, Yoo JJ. Association between inflammatory biomarkers and nutritional status in fatty liver. Clin Nutr Res. 2020; 9: 182-94.
[22] Choi WJ, Ford ES, Curhan G, Rankin JI, Choi HK. Independent association of serum retinol and beta-carotene levels with hyperuricemia: A national population study. Arthritis Care Res. 2012; 64: 389-96.
[23] Ruhl CE, Everhart JE. Fatty liver indices in the multiethnic United States National Health and Nutrition Examination Survey. Aliment Pharmacol Ther. 2015; 41: 65-76.
[24] Kim D, Kim W, Adejumo AC, Cholankeril G, Tighe SP, Wong RJ, Gonzalez SA, Harrison SA, Younossi ZM, Ahmed A. Race/ethnicity-based temporal changes in prevalence of NAFLD-related advanced fibrosis in the United States, 2005-2016. Hepatol Int. 2019; 13: 205-13.
[25] Kim D, Yoo ER, Li AA, Tighe SP, Cholankeril G, Harrison SA, Ahmed A. Depression is associated with non-alcoholic fatty liver disease among adults in the United States. Aliment Pharmacol Ther. 2019; 50: 590-8.
[26] Meffert PJ, Baumeister SE, Lerch MM, Mayerle J, Kratzer W, Völzke H. Development, external validation, and comparative assessment of a new diagnostic score for hepatic steatosis. Am J Gastroenterol. 2014, 109: 1404-14.
[27] Zhang P, Sun J, Guo Y, Han M, Yang F, Sun Y. Association between retinol intake and hyperuricaemia in adults. Public Health Nutr. 2021; 24: 2205-14.
[28] Sun Y, Sun J, Wang J, Gao T, Zhang H, Ma A. Association between vitamin C intake and risk of hyperuricemia in US adults. Asia Pac J Clin Nutr. 2018; 27: 1271-6.
[29] Feskanich D, Rimm EB, Giovannucci EL, Colditz GA, Stampfer MJ, Litin LB, Willett WC. Reproducibility and validity of food intake measurements from a semiquantitative food frequency questionnaire. J Am Diet Assoc. 1993; 93: 790-6.
[30] Hu FB, Rimm E, Smith-Warner SA, Feskanich D, Stampfer MJ, Ascherio A, Sampson L, Willett WC. Reproducibility and validity of dietary patterns assessed with a food-frequency questionnaire. Am J Clin Nutr. 1999; 69: 243-9.
[31] Menke A, Casagrande S, Geiss L, Cowie CC. Prevalence of and trends in diabetes among adults in the United States, 1988-2012. JAMA. 2015; 314: 1021-9.
[32] Whelton PK, Carey RM, Aronow WS, Casey DE, Jr., Collins KJ, Dennison Himmelfarb C, DePalma SM, Gidding S, Jamerson KA, Jones DW, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: A report of the American college of cardiology/American heart association task force on clinical practice guidelines. Hypertension. 2018; 71: e13-e115.
[33] Zeng J, Zhang J, Li Z, Li T, Li G. Prediction model of artificial neural network for the risk of hyperuricemia incorporating dietary risk factors in a Chinese adult study. Food & nutrition research. 2020; 64.
[34] Christensen K, Lawler T, Mares J. Dietary carotenoids and non-alcoholic fatty liver disease among US adults, NHANES 2003-2014. Nutrients. 2019; 11: 1101.
[35] Yoneda M, Mawatari H, Fujita K, Iida H, Yonemitsu K, Kato S, Takahashi H, Kirikoshi H, Inamori M, Nozaki Y, et al. High-sensitivity C-reactive protein is an independent clinical feature of nonalcoholic steatohepatitis (NASH) and also of the severity of fibrosis in NASH. J Gastroenterol. 2007; 42: 573-82.
[36] Abe RAM, Masroor A, Khorochkov A, Prieto J, Singh KB, Nnadozie MC, Abdal M, Shrestha N, Mohammed L. The role of vitamins in non-Alcoholic fatty liver disease: A systematic review. Cureus. 2021; 13: e16855.
[37] Iwaki M, Matsuda M, Maeda N, Funahashi T, Matsuzawa Y, Makishima M, Shimomura I. Induction of adiponectin, a fat-derived antidiabetic and antiatherogenic factor, by nuclear receptors. Diabetes. 2003; 52: 1655-63.
[38] Cimini FA, Barchetta I, Carotti S, Bertoccini L, Baroni MG, Vespasiani-Gentilucci U, Cavallo MG, Morini S. Relationship between adipose tissue dysfunction, vitamin D deficiency and the pathogenesis of non-alcoholic fatty liver disease. World J Gastroenterol. 2017; 23: 3407-17.
[39] Ma C, Liu Y, He S, Zeng J, Li P, Ma C, Ping F, Zhang H, Xu L, Li W, Li Y. Negative association between antioxidant vitamin intake and non-alcoholic fatty liver disease in Chinese non-diabetic adults: mediation models involving superoxide dismutase. Free Radic Res. 2020; 54: 670-7.
[40] Duseja A, Chalasani N. Epidemiology and risk factors of nonalcoholic fatty liver disease (NAFLD). Hepatol Int. 2013; 7 Suppl 2: 755-64.
[41] Musso G, Gambino R, De Michieli F, Cassader M, Rizzetto M, Durazzo M, Fagà E, Silli B, Pagano G. Dietary habits and their relations to insulin resistance and postprandial lipemia in nonalcoholic steatohepatitis. Hepatology. 2003; 37: 909-16.
[42] Marchesini G, Bugianesi E, Forlani G, Cerrelli F, Lenzi M, Manini R, Natale S, Vanni E, Villanova N, Melchionda N, Rizzetto M. Nonalcoholic fatty liver, steatohepatitis, and the metabolic syndrome. Hepatology. 2003; 37: 917-23.
[43] Zelber-Sagi S, Nitzan-Kaluski D, Goldsmith R, Webb M, Blendis L, Halpern Z, Oren R. Long term nutritional intake and the risk for non-alcoholic fatty liver disease (NAFLD): a population based study. J Hepatol. 2007; 47: 711-7.
[44] Sathiaraj E, Chutke M, Reddy MY, Pratap N, Rao PN, Reddy DN, Raghunath M. A case-control study on nutritional risk factors in non-alcoholic fatty liver disease in Indian population. Eur J Clin Nutr. 2011; 65: 533-7.
[45] Fan JG, Cao HX. Role of diet and nutritional management in non-alcoholic fatty liver disease. J Gastroenterol Hepatol. 2013; 28 Suppl 4: 81-7.
[46] Asrih M, Jornayvaz FR. Diets and nonalcoholic fatty liver disease: the good and the bad. Clin Nutr. 2014; 33: 186-90.
[47] Fan JG, Li F, Cai XB, Peng YD, Ao QH, Gao Y. Effects of nonalcoholic fatty liver disease on the development of metabolic disorders. J Gastroenterol Hepatol. 2007; 22: 1086-91.
[48] Jung HS, Chang Y, Kwon MJ, Sung E, Yun KE, Cho YK, Shin H, Ryu S. Smoking and the risk of non-alcoholic fatty liver disease: A cohort study. Am J Gastroenterol. 2019; 114: 453-63.
[49] Jia WP. The impact of cigarette smoking on metabolic syndrome. Biomed Environ Sci. 2013; 26: 947-52.
Cite This Article
  • APA Style

    Liu, C., Bai, Z., Cheng, J. (2025). Plant-Based Retinol Intake and Risk of Nonalcoholic Fatty Liver Disease in American Adults: Insights from NHANES 2007-2014. World Journal of Public Health, 10(3), 379-388. https://doi.org/10.11648/j.wjph.20251003.29

    Copy | Download

    ACS Style

    Liu, C.; Bai, Z.; Cheng, J. Plant-Based Retinol Intake and Risk of Nonalcoholic Fatty Liver Disease in American Adults: Insights from NHANES 2007-2014. World J. Public Health 2025, 10(3), 379-388. doi: 10.11648/j.wjph.20251003.29

    Copy | Download

    AMA Style

    Liu C, Bai Z, Cheng J. Plant-Based Retinol Intake and Risk of Nonalcoholic Fatty Liver Disease in American Adults: Insights from NHANES 2007-2014. World J Public Health. 2025;10(3):379-388. doi: 10.11648/j.wjph.20251003.29

    Copy | Download

  • @article{10.11648/j.wjph.20251003.29,
      author = {Can Liu and Zeming Bai and Jingmin Cheng},
      title = {Plant-Based Retinol Intake and Risk of Nonalcoholic Fatty Liver Disease in American Adults: Insights from NHANES 2007-2014
    },
      journal = {World Journal of Public Health},
      volume = {10},
      number = {3},
      pages = {379-388},
      doi = {10.11648/j.wjph.20251003.29},
      url = {https://doi.org/10.11648/j.wjph.20251003.29},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.wjph.20251003.29},
      abstract = {Existing evidence suggests a strong correlation between nonalcoholic fatty liver disease (NAFLD) risk and dietary factors, and this investigation aimed to examine the association between dietary factors and NAFLD risk in American adults. Utilizing data from the National Health and Nutrition Examination Survey (NHANES) conducted between 2007 and 2014, the study employed chi-square tests of independence and t-tests to analyze differences between the NAFLD and control groups, while logistic regression analysis was used to identify factors influencing NAFLD risk and assess the association of plant-based dietary retinol intake with such risk. The NAFLD group consisted of 1,286 males (53.5%) and 1,138 females (46.9%), and logistic regression analysis identified uric acid (UA), high-density lipoprotein (HDL), smoking, vigorous recreational activity, hypertension, diabetes, gender, BMI, race, annual household income, and plant-based retinol intake as significant predictors of NAFLD (P < 0.05), with notably higher dietary intake of plant-based retinol being associated with a lower risk of NAFLD (OR = 0.670, 95% CI: 0.532-0.842). This study demonstrates that specific dietary components, especially plant-based retinol, play an important role in influencing NAFLD risk among American adults, and further long-term research is needed to inform public health initiatives aimed at reducing NAFLD prevalence.
    },
     year = {2025}
    }
    

    Copy | Download

  • TY  - JOUR
    T1  - Plant-Based Retinol Intake and Risk of Nonalcoholic Fatty Liver Disease in American Adults: Insights from NHANES 2007-2014
    
    AU  - Can Liu
    AU  - Zeming Bai
    AU  - Jingmin Cheng
    Y1  - 2025/09/05
    PY  - 2025
    N1  - https://doi.org/10.11648/j.wjph.20251003.29
    DO  - 10.11648/j.wjph.20251003.29
    T2  - World Journal of Public Health
    JF  - World Journal of Public Health
    JO  - World Journal of Public Health
    SP  - 379
    EP  - 388
    PB  - Science Publishing Group
    SN  - 2637-6059
    UR  - https://doi.org/10.11648/j.wjph.20251003.29
    AB  - Existing evidence suggests a strong correlation between nonalcoholic fatty liver disease (NAFLD) risk and dietary factors, and this investigation aimed to examine the association between dietary factors and NAFLD risk in American adults. Utilizing data from the National Health and Nutrition Examination Survey (NHANES) conducted between 2007 and 2014, the study employed chi-square tests of independence and t-tests to analyze differences between the NAFLD and control groups, while logistic regression analysis was used to identify factors influencing NAFLD risk and assess the association of plant-based dietary retinol intake with such risk. The NAFLD group consisted of 1,286 males (53.5%) and 1,138 females (46.9%), and logistic regression analysis identified uric acid (UA), high-density lipoprotein (HDL), smoking, vigorous recreational activity, hypertension, diabetes, gender, BMI, race, annual household income, and plant-based retinol intake as significant predictors of NAFLD (P < 0.05), with notably higher dietary intake of plant-based retinol being associated with a lower risk of NAFLD (OR = 0.670, 95% CI: 0.532-0.842). This study demonstrates that specific dietary components, especially plant-based retinol, play an important role in influencing NAFLD risk among American adults, and further long-term research is needed to inform public health initiatives aimed at reducing NAFLD prevalence.
    
    VL  - 10
    IS  - 3
    ER  - 

    Copy | Download

Author Information