1. Introduction

Nonalcoholic fatty liver disease (NAFLD), a common chronic liver disease, a global prevalence of NAFLD was estimated to be 30.2% (95% CI: 28.7%–31.7%) [1]. The main cause of NAFLD is the development of metabolic syndrome in the body, which is associated with insulin resistance, obesity, and hyperlipidemia in the body [2]. Obesity and insulin resistance often lead to chronic inflammation; therefore, patients with NAFLD generally have chronic inflammation accompanying them. NAFLD is a part of the progression of liver disease that begins with steatosis in the liver and progresses to nonalcoholic steatohepatitis (NASH), which, without intervention, will proceed to the next step of advanced fibrosis, which may eventually lead to cirrhosis or even hepatocellular carcinoma. Early identification and intervention are particularly important given the adverse consequences of all of the above [3, 4].

Increased oxidative stress and inflammation induced by fatty deposits are considered to be the main drivers of hepatic and extrahepatic injury [5, 6]. On this basis, NAFLD is gradually undergoing development. There is no definitive drug that can successfully treat NAFLD, so new ways of treating NAFLD are constantly being explored in addition to drug treatment modalities. Numerous studies have reported that ingredients in many foods can reduce the risk of developing inflammation-related diseases [7–11]. There is a growing awareness of the importance of adopting good lifestyle habits to prevent or improve the development of diseases, and that liver diseases caused by fatty deposits can be prevented by losing weight or improving the quality of the diet. Diet and nutrition are increasingly recognized as major modifiable determinants of liver health and metabolic homeostasis [12]. Diet is a modifiable environmental factor that plays an important role in regulating inflammation and immune function, among other things. Previous studies have demonstrated that foods with anti-inflammatory properties, such as tea, vegetables, and nuts, can reduce the risk of developing rheumatoid arthritis [13, 14]. In addition, a summary of recent research on inflammatory diets and chronic diseases, such as diabetes and cardiovascular disease, found that diets with inflammatory features were strongly associated with the onset and severity of chronic diseases, and that some of these associations were gender-related [15]. In the face of a rich diet, rational choices play a vital role in promoting good health. By validating in vivo and in vitro models, Gao et al. [16] found that dietary intervention could enhance hepatic lipoautophagy by inhibiting the Akt/mTOR/ULK1 pathway and demonstrated for the first time that lipid accumulation increases hepatic senescence, and that hepatic senescence implies a decline in function, on the basis of which NAFLD is further progressed. Diet has a role in regulating inflammation, and making the right dietary choices can reduce inflammation in the body to a certain extent and even provide anti-inflammatory effects [17].

Dietary Inflammatory Index (DII) is a scoring mechanism derived from the literature to assess the inflammatory potential of diets and to link diet to inflammation [18]. The DII has been widely studied as a tool for measuring the inflammatory potential of diets [19–22]. The advantage of the DII over other diet quality scoring tools is that it has been validated against circulating concentrations of C-reactive protein (CRP) and other systemic markers of inflammation [18, 23].

The present study utilized data from the National Health and Nutrition Examination Survey (NHANES) database to assess the inflammatory potential of participants’ diets through DII in order to investigate the effect of DII on NAFLD, and the effects of different factors on NAFLD, and to provide a theoretical basis for the prevention and treatment of NAFLD in life.

2. Methods

2.1. Study Population

The NHANES database in the United States is responsible for compiling life and health statistics data [24]. NHANES collects data primarily through demographic, dietary, physical measurements, laboratory tests, and questionnaires. Due to the continuous updating of the NHANES database’s inspection items, the outcome variables collected in this study have been collected since 2017. Therefore, the data collection and sample size determination have also been carried out since 2017. The final year we selected for inclusion in the population was 2017–2018. We excluded those with missing controlled attenuation parameter (CAP) score and DII (n = 10443), covariate (n = 459) information. Patients with other causes of chronic liver disease has also been excluded (n = 2194), including liver cancer, autoimmune hepatitis, hepatitis B disease, hepatitis C disease and heavy drinking (≥3 drinks/day for females, ≥4 drinks/day for males, or binge drinking ≥5 days/month) [25]. Finally, a total of 8708 participants were included in this study (Figure 1).

3. Results

3.3. DII is Independently Associated With NAFLD

Multivariate logistic regression analyses of DII and NAFLD are shown in Table 2. In Model 1, the risk of NAFLD for participants with DII < 0 was 0.84 times higher than for those with DII > 0. The same trend was observed in Model 3, which adjusted for age, gender, race, marital, education, smoking, diabetes, Hypertension, HDL-cholesterol, and triglyceride, with the risk increasing to 0.85 times.

Table 2. Association between DII and NAFLD.

Variable	Number of events	Model 1		Model 2		Model 3
		95% CI	p	95% CI	p	95% CI	p
Dietary inflammation index
Proinflammation (DII ≥ 0)	6839	Ref	—	Ref	—	Ref	—
Anti-inflammation (DII < 0)	1869	0.84 (0.73,0.96)	0.02	0.71 (0.62,0.83)	<0.0001	0.85 (0.73,0.99)	0.04
p for trend	—	—	0.02	—	<0.0001	—	0.04

• Note: Model 1: unadjusted model. Model 2: adjustment for age, gender and race. Model 3: adjustment for age, gender, race, marital, education, smoking, diabetes, Hypertension, HDL-cholesterol and triglyceride.
• Abbreviations: CI, confidence interval; OR, odd ratio; Ref, reference.

The RCS showed a nonlinear relationship between DII and NAFLD, with events of NAFLD increasing with DII (Figure 2).

3.4. Subgroup Analysis

We found a significant interaction between DII and gender and race (p  < 0.05). The positive association between DII and NAFLD appeared stronger in elderly people (aged > 60 years; OR: 1.51; 95% CI: 1.10–2.07); females (OR: 1.43; 95% CI: 1.11–1.85); and whites (OR: 1.37; 95% CI: 1.12–1.68) (Figure 3).

4. Discussion

This study delves into the connection between the DII and NAFLD. Our findings reveal a significant link between a proinflammatory diet and an increased risk of NAFLD. Moreover, the most notable correlation between DII and NAFLD emerged among Caucasian women aged over 60 years.

The results of the previous study were similar to the current one, but slightly different. In the study by Tyrovolas et al. [28], four equations were used instead of the diagnosis of NAFLD, and the inflammatory index of diet was not estimated through DII, but through the dietary anti-inflammatory index (D-ALL), which is not a widely recognized scale. Therefore, it seems more prudent to choose DII for estimation purposes. There are also cohort studies by Valibeygi et al. [29] that differ from ours. The NAFLD diagnostic criteria used in the study are currently appropriate. Although liver biopsy is the gold standard for diagnosis, this is not realistic for routine screening of our disease. Vibration-controlled transient elastography (VCTE) is a noninvasive imaging method that can more accurately detect steatosis when it occurs in the liver, and has been widely used in previous studies for the diagnosis of NAFLD [27, 30, 31]. That anti-inflammatory diets are associated with a low incidence of inflammatory diseases seems to be known as common sense, but different parts of the body have different inflammatory mechanisms. Some previous studies have attempted to explain how inflammation in the liver arises. Ahmed et al. suggested that when excessive dietary intake is not consumed in a timely manner, it is converted to fat. Excess free fatty acids and dietary lipids enter the liver and can be deposited as ectopic fat and become lipotoxic, leading to damage to organelles in hepatocytes, and the dysregulated organelles release excessive reactive oxygen species (ROS) and proinflammatory cytokines, leading to systemic inflammation [32]. Excessive intake of proinflammatory diets like high-sugar, high-carbon-water foods, processed meats, etc., are generally converted to fat, and the process described above occurs to drive inflammation in the liver, which in turn leads to NAFLD. Strate et al. [33] found that a proinflammatory diet may lead to chronic low-grade systemic inflammation, which may contribute to the development of NAFLD. This inflammation may be mediated by proinflammatory factors, such as ferritin and CRP [34], and gut microbes may also mediate the link between a proinflammatory diet and NAFLD [35].

Previous research has extensively explored the anti-inflammatory properties of various diets, often utilizing CRP levels as a marker of inflammation. Certain dietary patterns, such as those rich in whole grains [36], fruits, and vegetables [37], have demonstrated the ability to decrease inflammation, as evidenced by lower serum CRP levels. These diets are distinguished by their high content of vitamins, phytochemicals, and fiber. Moreover, consumption of dairy products among animal foods has been associated with a notable reduction in CRP levels [38]. Examining a specific nutrient can offer insights into the impact of individual dietary components on inflammation. However, in real-world dietary contexts, the composition is intricate, with potential interactions between various foods that may act synergistically or antagonistically. Nealed et al. illustrated that adherence to the Mediterranean diet led to a reduction in CRP levels [39]. Similarly, Soltani et al. [40] investigation into the dietary approaches to stop hypertension (DASH) yielded comparable findings. The Mediterranean diet is rich in antioxidants like polyphenols, which play a role in modulating oxidative stress and metabolic inflammation mediated by nicotinamide adenine dinucleotide phosphate oxidase (NADPH) and NF-κB. Additionally, these polyphenols efficiently upregulate the downstream effectors of various proteins, particularly adenosine 5‘-monophosphate (AMP)-activated protein kinase (AMPK). Phosphorylation of AMPK mitigates oxidative stress and inflammation throughout the body, as indicated primarily by decreased production of ROS, proinflammatory cytokines, and adhesion molecule expression [41].

A notable strength of this study lies in the adoption of a contemporary and rational diagnostic tool for NAFLD diagnosis: VCTE. Previous studies relied on ultrasound and liver enzyme tests [42, 43], which are deemed unreliable for detecting liver fibrosis and may introduce misclassification bias. The second strength lies in the utilization of data from NHANES, which employs a robust sampling methodology representative of the population, ensuring broad-reaching conclusions. However, this study has limitations. The dietary data used for calculating the DII were derived from participants’ dietary recalls spanning two 24-h periods. While generally consistent, these may deviate from actual dietary habits. Furthermore, despite efforts to control for confounders, unmeasured variables from the NHANES database had to be excluded.

5. Conclusion

The study findings revealed an association between DII and the risk of developing NAFLD, with the risk escalating proportionally as DII increased. Dietary management emerges as a crucial strategy in liver disease prevention, particularly for NAFLD.

Ethics Statement

The survey protocols were approved by the National Center for Health Statistics Research Ethics Review Board.

Consent

Written informed consent was obtained from every participant.

Disclosure

NHANES is a publicly available dataset without personal identifiable information and has been used by researchers worldwide.

Conflicts of Interest

The authors declare no conflicts of interest.

Author Contributions

Conception and design of the study: Jinxi Wang and Dawei Ye. Literature review and analysis: Wei Zhang and Jinghan Jia. Drafting and critical revision: Yuan He, Jinxi Wang, and Dawei Ye. Editing: Yuan He. Final approval of the final version: Jinxi Wang and Dawei Ye. Yuan He and Yuhang Yang are the co-first author.

Funding

This work was not funded.