Comparison of Dietary Inflammatory Index, Physical Activity Level, and Dietary Macronutrient Intake between Newly Diagnosed Atherosclerotic Patients and Healthy Controls

1. INTRODUCTION

Cardiovascular disease (CVD) is the leading cause of mortality worldwide [1]. Low-grade inflammation of the endothelium is a primary underlying pathologic basis of atherosclerotic cardiovascular disease (ASCVD) [2], where reactive oxygen species and inflammatory cytokines play a substantial role [3]. This inflammatory activity may lead to endothelial dysfunction [4].

Certain dietary factors have been suggested as risk factors for atheroma development, either directly or indirectly through other risk factors, such as plasma lipids and glucose [5]. Healthy dietary patterns, combined with portion control and energy balance, have been proposed to reduce excess weight gain and CVD risk [6, 7].

A substantial body of research demonstrates associations between dietary patterns and inflammation regulation via proinflammatory cytokines, suggesting a modulatory role in atherogenesis [8, 9]. Given the significant role of inflammation in ASCVD and its potential modulation through diet, categorizing an individual's diet based on its inflammatory properties may provide valuable insights into the relationships among diet, inflammation, and CVD [10]. The Dietary Inflammatory Index (DII) is a validated tool for assessing the inflammatory potential of the diet and its association with CVD incidence [11]. Studies indicate that individuals with higher (more proinflammatory) DII scores have a higher incidence of CVD and worse cardiometabolic risk profiles, with associations observed for coronary heart disease, stroke, and elevated inflammatory biomarkers [12-17]. This supports the concept that diet-driven systemic inflammation contributes to ASCVD risk.

Some evidence further suggests that DII may be linked to CVD and CVD-related mortality [10, 12, 18-22]. To strengthen this evidence, we conducted a case-control study in Hamadan City, Iran, in 2024, comparing DII and physical activity level (PAL) between individuals with newly diagnosed ASCVD and age- and sex-matched healthy controls, and evaluating the association between DII and ASCVD. We hypothesized that patients with ASCVD would exhibit higher DII scores and lower PAL compared with healthy controls.

2. MATERIALS AND METHODS

This case-control study included 103 newly diagnosed (within the recent three months) ASCVD patients in Hamadan City (Iran) as the case group and 103 healthy controls. The controls were selected among friends or neighbors of each ASCVD patient, ensuring gender matching and a similar age range (±5 years).

The inclusion criteria for the case group required a definitive diagnosis of ASCVD [23, 24] by cardiologists within the past three months, along with non-adherence to a prescribed diet or significant changes in dietary habits during the three months preceding the study.

All participants completed a 168-item food frequency questionnaire (FFQ) [25]. Calorie, carbohydrate, protein, total fat, saturated fatty acids (SFA), monounsaturated fatty acids (MUFA), polyunsaturated fatty acids (PUFA), and dietary fiber intake were estimated using ShaFA software [26] based on the FFQ data.

The DII for each participant was calculated using the methodology proposed by Shivappa et al. [11]. Due to the absence of dietary intake data for specific components, only 38 of the original 45 food parameters were included in the computation. Specifically, eugenol, flavan-3-ol, flavones, flavonones, flavonols, anthocyanidins, and isoflavones were not included.

Physical activity was assessed at two levels using two researcher-made questions:

• Level 1: No exercise or regular walking.

• Level 2: One or more sessions of exercise or regular walking per week.

3. RESULTS

A total of 103 newly diagnosed ASCVD patients and 103 healthy controls were included in the study. No significant differences were observed between the two groups in dietary energy, protein, or cholesterol intake. However, ASCVD patients had higher dietary intakes of total fat, saturated fatty acids (SFA), polyunsaturated fatty acids (PUFA), and monounsaturated fatty acids (MUFA), as well as higher Dietary Inflammatory Index (DII) scores compared with the control group. In contrast, dietary intake of carbohydrates and fiber was higher in the control group (Table 1).

In the multiple logistic regression model, which included dietary intake of protein, carbohydrates, fiber, and total fat, dietary total fat (p<0.001) and fiber (p=0.005) were significant predictors of ASCVD incidence (Table 2).

Logistic regression analysis revealed that a one-unit increase in the Dietary Inflammatory Index (DII) was associated with a 16.8% increase in the risk of developing ASCVD (Odds Ratio [OR]: 1.167; 95% Confidence Interval [CI]: 1.008–1.352, p=0.039).

There was a significant difference in physical activity level (PAL) between the two groups (Table 3). Compared with activity level one (no exercise or regular walking), activity level two (one or more sessions of exercise or regular walking per week) was associated with a 50.2% reduction in the risk of ASCVD incidence (OR: 0.498; 95% CI: 0.265–0.934, p=0.03).

Participants were divided into two subgroups based on their DII scores (≤1 and >1). Logistic regression analysis within these subgroups showed that higher PAL was associated with a reduced risk of ASCVD only in the group with DII ≤1 (OR: 0.152; 95% CI: 0.032–0.724, p=0.018), whereas in the group with DII >1, higher PAL had no significant effect on ASCVD prevention (OR: 0.652; 95% CI: 0.298–1.426, p=0.284).

4. DISCUSSION

In this study, dietary intakes of total fat, saturated fatty acids (SFA), polyunsaturated fatty acids (PUFA), monounsaturated fatty acids (MUFA), and Dietary Inflammatory Index (DII) scores were higher in ASCVD patients compared with the control group. In contrast, dietary intake of carbohydrates and fiber was higher in the control group. Additionally, higher physical activity level (PAL) was associated with a lower risk of ASCVD development.

The incidence of non-communicable diseases is significantly influenced by diet [27] and diet-related metabolites [28]. Among the modifiable risk factors for CVD (i.e., metabolic, environmental, and behavioral), dietary factors rank highest. It has been estimated that dietary risk factors contribute to 53% of CVD deaths and 58% of CVD-related disabilities [29].

Numerous dietary patterns have been proposed to reduce CVD events, including diets low in total or saturated fats [30, 31]. For example, a meta-analysis found that Mediterranean diet and low-fat dietary programs probably reduce the risk of mortality and myocardial infarction [32]. In our study, dietary intake of total fat, SFA, PUFA, and MUFA was higher in patients with ASCVD than in the control group, indicating that higher fat intake, even of unsaturated types, is associated with a higher risk of developing ASCVD. This suggests that total dietary fats may act as an independent risk factor for CVD regardless of fatty acid type. However, some studies suggest that substituting SFA with PUFA and MUFA may decrease CVD risk [33-36].

Conversely, increased consumption of whole grains, nuts, seeds, beans, legumes, fruits, and vegetables (which are fiber-rich sources), as well as fish, lean meats, and low-fat dairy products, contributes to lower CVD mortality [37-49].

Currently, it is believed that dietary cholesterol has a limited impact on serum low-density lipoprotein (LDL) cholesterol levels and the risk of CVD compared with other dietary and lifestyle factors. A recent study involving over 17,700 participants from 50 countries supported this perspective, showing no significant association between egg consumption and increased blood lipids, blood pressure, or CVD-related mortality [50]. Similarly, in our study, no significant differences were observed between the two groups in terms of cholesterol intake, supporting the view that dietary cholesterol may not significantly affect CVD incidence.

In the present study, foods higher in carbohydrates and fiber demonstrated a protective effect against ASCVD, consistent with previous studies highlighting the benefits of fiber-rich foods, such as whole grains, vegetables, and fruits [51-55]. This protective effect may be mediated through alterations in the gut microbiota, promoting fiber fermentation and short-chain fatty acid (SCFA) production [56, 57].

The association of DII with CVD incidence has been examined in several studies. Analysis of data from the National Health and Nutrition Examination Survey (NHANES) revealed a direct association between the 28-item DII and the risk of ASCVD development, which was more pronounced in women [58]. However, dietary intake in this study was based on a single 24-hour dietary recall, which may not accurately reflect dietary fluctuations. A similar finding was observed in the Prevención con Dieta Mediterránea (PREDIMED) study, where CVD risk increased across DII quartiles [20]. Furthermore, following over 18,000 Spanish university graduates for 8.9 years, the Seguimiento Universidad de Navarra (SUN) Cohort study found that participants in the highest DII quartile were at approximately twice the risk of CVD incidence compared with those in the lowest quartile [21]. A meta-analysis also suggested that each unit increase in the DII increases CVD risk by 8% [19]. Conversely, studies conducted in Iran [59] and Australia [23] found no association between DII and CVD.

In the present study, each unit increase in the DII was associated with a 16.8% increase in the risk of developing ASCVD. Moreover, at higher DII levels, even higher physical activity levels (PAL) did not prevent the incidence of ASCVD.

Many studies indicate that adequate physical activity level (PAL) can prevent or delay CVD. PAL significantly lowers CVD risk by reducing serum triglycerides, increasing serum high-density lipoprotein (HDL) cholesterol, and decreasing coronary artery calcium [60, 61]. In our study, higher PAL was associated with a lower risk of ASCVD, and this protective effect was more pronounced in individuals with lower Dietary Inflammatory Index (DII) scores.

Certain variables, including carbohydrate, total fat, saturated fat, fiber intake, and DII, did not show statistically significant differences within the female subgroup, despite reaching significance in the male subgroup. This discrepancy may reflect genuine gender-based physiological differences or may be attributable to limited statistical power in the subgroup analysis.

The limitations of this study include the lack of use of validated PAL questionnaires, such as the International Physical Activity Questionnaire (IPAQ), due to the potential for a low participation rate, as anthropometric assessment and completion of the FFQ were time-consuming and tedious. Another limitation is recall bias, which is inherent in retrospective questionnaires such as the FFQ. Additionally, the number of participants, particularly in subgroup analyses, was relatively small.

CONCLUSION

Our findings support the notion that patients with ASCVD consumed higher amounts of fat and exhibited a proinflammatory dietary pattern. In contrast, the control group showed higher intakes of carbohydrates and fiber. Furthermore, increased PAL was associated with a decreased risk of ASCVD. Future studies with larger sample sizes and different ethnicities are required.

REFERENCES