Introduction
According to the Japanese Society of Psychosomatic Medicine, psychosomatic illness refers to any organic or functional damage as a result of psychological disorders [
1]. Psychosomatic illness has a substantial effect on quality of life [
2,
3]. In view of the growing prevalence of psychological disorders [
4], along with their large impacts on medical history of diseases, it is necessary to identify new approaches to prevent psychological disorders and their medical complications, or delay their progression.
Peripheral and central inflammatory pathways have been positively linked to mental disorders [
5], as has functional damage in somatization [
6]. Recent evidence suggests that nutritional interventions can be considered as a mainstream approach in psychiatric practice [
7,
8]. Recently, results of a meta-analysis have shown that a ‘healthy dietary pattern’, characterized by whole grains, fruits and vegetables, is associated with a lower risk of depression and anxiety, whereas an ‘unhealthy dietary pattern’, which consisted of red or processed meats, refined grains, and high-sugar or high-fat foods, is associated with an increased risk of mental disorders [
9].
In addition, various bioactive components in the diet may exert pro- or anti-inflammatory effects [
10]. Therefore, pro-inflammatory features of an unhealthy dietary pattern may underpin chronic inflammation [
11‐
13], psychological disorders [
14], and probably psychosomatic complaints. Several investigations have evaluated the relation between the dietary inflammatory index (DII), reflective of the potential pro-inflammatory properties of a diet, with psychological disorders, with most indicating a direct link between DII and the risk of psychological disorders [
15‐
22].
In a recent analysis based on data from the SEPAHAN project, and consistent with earlier publications [
15‐
22], we found that higher DII scores were associated with an increased risk of having higher psychological disorders profile scores (including depression, anxiety and psychological distress) [
23]. Moreover, in another study in this population, we found that a healthy dietary pattern was inversely associated with the risk of all identified psychosomatic, including psychological, gastrointestinal, neuro-skeletal and pharyngeal-respiratory somatic, complaints, whilst greater adherence to the Western (unhealthy) dietary pattern was associated with a greater risk of psychological somatic complaints [
24].
Although several studies have assessed the relation between DII and psychological disorders, we are not aware of any study investigating the relation between DII and psychosomatic complaints profiles. Due to the considerable impact of psychological status on organic and functional disorders, as well as the effect of diet and inflammation on mood status, we hypothesized that a pro-inflammatory diet may influence somatic complaints by affecting mood status. Therefore, the current study was conducted to examine the association between the dietary inflammatory index and psychosomatic complaints profiles in a large sample of Iranian adults.
Results
Table
1 shows age-, sex- and energy-adjusted dietary intakes of the study population according to tertiles of DII. Compared with those in the lowest tertile, those in the highest tertile of DII had greater intakes of energy, fat, caffeine, hydrogenated vegetable oils, and refined grains, but lower intakes of carbohydrate, protein, fiber, folate, pyridoxine, magnesium, fruit, vegetables, nuts, legumes and soy, red and white meats and whole grains.
Table 1
Dietary intakes of the participants across tertiles of the dietary inflammatory index1
n | 939 | 940 | 939 | |
Energy (kcal/d) | 2040.02 ± 25.94 | 2273.71 ± 25.67 | 2844.32 ± 26.05 | < 0.0001 |
Carbohydrate (% of total daily energy) | 50.64 ± 0.28 | 48.41 ± 0.27 | 48.42 ± 0.29 | < 0.0001 |
Fat (% of total daily energy) | 36.30 ± 0.23 | 38.07 ± 0.22 | 38.18 ± 0.24 | < 0.0001 |
Protein (% of total daily energy) | 15.29 ± 0.08 | 14.93 ± 0.08 | 14.22 ± 0.08 | < 0.0001 |
Fiber (g/d) | 27.12 ± 0.16 | 22.96 ± 0.16 | 17.67 ± 0.17 | < 0.0001 |
Caffeine (mg/d) | 88.37 ± 3.27 | 96.49 ± 3.14 | 112.97 ± 3.37 | < 0.0001 |
Total folate intake (μg/d) | 604.36 ± 4.28 | 569.21 ± 4.11 | 549.68 ± 4.41 | < 0.0001 |
Vitamin B6 (mg/d) | 2.24 ± 0.01 | 2.01 ± 0.01 | 1.69 ± 0.01 | < 0.0001 |
Vitamin B12 (μg/d) | 2.99 ± 0.04 | 3.00 ± 0.04 | 2.90 ± 0.04 | 0.101 |
Mg (mg/d) | 366.34 ± 1.68 | 333.74 ± 1.61 | 284.99 ± 1.73 | < 0.0001 |
Omega-3 fatty acids (g/d) | 2.28 ± 0.04 | 2.25 ± 0.04 | 2.23 ± 0.04 | 0.648 |
Food groups |
Fruit (g/d) | 452.98 ± 7.53 | 311.71 ± 7.23 | 196.13 ± 7.76 | < 0.0001 |
Vegetables (g/d) | 322.29 ± 3.74 | 235.29 ± 3.59 | 161.13 ± 3.85 | < 0.0001 |
Nuts, legumes and soy (g/d) | 65.72 ± 1.24 | 58.79 ± 1.19 | 43.07 ± 1.27 | < 0.0001 |
White meat (g/d) | 66.27 ± 1.55 | 64.54 ± 1.48 | 60.46 ± 1.59 | 0.039 |
Red meat (g/d) | 83.02 ± 1.40 | 82.09 ± 1.35 | 69.79 ± 1.44 | < 0.0001 |
Hydrogenated vegetable oil (g/d) | 9.67 ± 0.38 | 10.52 ± 0.37 | 11.36 ± 0.39 | 0.014 |
Refined grains (g/d) | 338.03 ± 5.67 | 375.38 ± 5.44 | 460.88 ± 5.84 | < 0.0001 |
Whole grains (g/d) | 57.00 ± 2.69 | 51.73 ± 2.58 | 23.19 ± 2.77 | < 0.0001 |
Table
2 shows the individual somatic complaints factor loading matrix for each of the four psychosomatic complaints. Each psychosomatic complaint profile was labeled based on individual somatic complaints which were highly loaded. For example, disorders related to feelings, thoughts, and sleep were captured in the ′psychological′ somatic complaints profile, complaints related to the gastrointestinal tract, including nausea, diarrhea, and bloating, in the ′gastrointestinal′ profile, back, neck, and joint pain in the ′neuro-skeletal′ profile, and disorders relating to the pharyngeal and respiratory systems, such as shortness of breath, hoarseness and wheezing, in the ′pharyngeal-respiratory′ profile. The ′psychological′ somatic complaints explained 12.7% of the total variance. Corresponding values for ′gastrointestinal′, ′neuro-skeletal′, and ′pharyngeal-respiratory′ were 11.7, 11.6, and 8.9%, respectively [
37,
38]. The correlation coefficients of the identified psychosomatic complaints profiles with DII and its individual components are shown in Additional file
1: Table S1. In most cases, correlation coefficients were greater for DII compared with correlations for its components. However, correlations between all four psychosomatic complaints and vitamin C were constantly greater than those for DII; therefore, the risk of psychosomatic complaints were assessed across the tertiles of vitamin C intake (Additional file
1: Table S2). In spite of an inverse association between vitamin C intake and all four somatic complaints in the crude model, the associations remained significant only for pharyngeal-respiratory somatic complaints and showed a trend towards lower risk for psychological and gastrointestinal somatic complaints in the fully-adjusted model.
Table 2
Factor loadings for the four extracted somatic complaints profiles from 31 somatic complaints
Somatic complaints | Factor loadings a |
Psychological | Gastrointestinal | Neuro-skeletal | Pharyngeal-respiratory |
Sleep disorder |
0.420
| 0.148 | 0.325 | 0.154 |
Pounding heart |
0.577
| 0.129 | 0.300 | 0.236 |
Feeling low on energy |
0.565
| 0.163 | 0.416 | 0.014 |
Feeling like ′butterflies′ in the stomach |
0.869
| 0.242 | 0.110 | 0.167 |
Difficulty concentrating |
0.869
| 0.242 | 0.110 | 0.167 |
Disturbing thoughts |
0.664
| 0.144 | 0.261 | 0.036 |
Dry mouth | 0.103 |
0.248
| 0.236 | 0.220 |
Chest pain | 0.339 |
0.454
| 0.087 | 0.233 |
Feeling of fullness | 0.259 |
0.662
| 0.139 | 0.132 |
Nausea | 0.283 |
0.509
| 0.047 | 0.262 |
Gastroesophageal reflux | 0.153 |
0.544
| 0.012 | 0.318 |
Pain or discomfort in the abdomen | 0.239 |
0.678
| 0.206 | 0.139 |
Constipation | 0.070 |
0.512
| 0.255 | −0.037 |
Diarrhea | −0.061 |
0.374
| 0.235 | 0.124 |
Bloating or swelling of the abdomen | 0.210 |
0.644
| 0.288 | 0.022 |
Anal pain | 0.122 |
0.473
| 0.239 | 0.183 |
Headache | 0.246 | 0.239 |
0.547
| 0.134 |
Back pain | 0.139 | 0.168 |
0.661
| 0.148 |
Pain in joints | 0.230 | 0.170 |
0.612
| 0.160 |
Eyesore | 0.207 | 0.075 |
0.461
| 0.301 |
Severe fatigue | 0.361 | 0.185 |
0.646
| 0.081 |
Dizziness and confusion | 0.343 | 0.245 |
0.513
| 0.254 |
Chills and extreme cold | 0.158 | 0.175 |
0.435
| 0.346 |
Hot flashes | 0.274 | 0.279 |
0.350
| 0.146 |
Menstrual disorder | −0.038 | 0.323 |
0.389
| −0.021 |
Neck pain | 0.105 | 0.154 | 0.322 |
0.570
|
Globus sensation | 0.165 | 0.372 | 0.015 |
0.510
|
Having trouble swallowing | 0.090 | 0.240 | −0.021 |
0.596
|
Shortness of breath | 0.391 | 0.124 | 0.311 |
0.492
|
Hoarseness | 0.015 | 0.092 | 0.225 |
0.612
|
Wheezing (asthma) | 0.104 | 0.000 | 0.124 |
0.567
|
Variance explained (%) | 12.70 | 11.73 | 11.55 | 8.85 |
Cumulative variance | 12.70 | 24.43 | 35.99 | 44.84 |
Participant characteristics across the tertiles of DII are presented in Table
3. Participants with the highest DII scores, reflecting a more pro-inflammatory diet, were more likely to be younger, male, and current smokers, whilst those in the lowest tertile were more likely to be physically active and overweight or obese. Marital status and education levels did not differ across the tertiles of DII.
Table 3
General characteristics of the study participants across tertiles of the dietary inflammatory index1
n | 939 | 940 | 939 | |
Age (years) | 37.6 ± 0.3 | 36.0 ± 0.3 | 35.4 ± 0.3 | < 0.0001 |
BMI (kg/m2) | 25.5 ± 0.2 | 24.9 ± 0.1 | 24.7 ± 0.1 | < 0.0001 |
Male (%) | 34.0 | 40.7 | 48.1 | < 0.0001 |
Married (%) | 83.3 | 81.2 | 78.5 | 0.121 |
Educational level (%) | | | | 0.888 |
≤12 yrs | 11.6 | 10.0 | 10.3 | |
12–16 yrs | 80.3 | 82.1 | 81.2 | |
> 16 yrs | 8.1 | 7.8 | 8.4 | |
Physically active (%) | 52.4 | 44.9 | 41.2 | < 0.0001 |
Overweight or obese3 (%) | 51.3 | 45.2 | 43.8 | 0.003 |
Current smokers (%) | 13.5 | 12.4 | 14.1 | 0.020 |
Logistic regression analysis (Table
4) indicated that, in the crude model, individuals in the top tertile of DII had a greater risk of having higher scores for psychological (OR = 1.40, 95% CI: 1.16, 1.69;
P < 0.0001), neuro-skeletal (OR = 1.35, 95% CI: 1.06, 1.73;
P = 0.019), and pharyngeal-respiratory (OR = 1.22, 95% CI: 1.01, 1.48;
P = 0.035) somatic complaints compared with those in the first tertile, while, despite a trend towards a higher risk of having greater scores for gastrointestinal somatic complaints with a more pro-inflammatory diet, the association did not reach significance (OR = 1.22, 95% CI: 0.99, 1.49;
P = 0.058). Adjustment for age, sex, and energy intake, lifestyle factors and BMI strengthened the risk of having higher scores of psychological (OR = 1.65, 95% CI: 1.29, 2.12;
P < 0.0001), gastrointestinal (OR = 1.49, 95% CI: 1.14, 1.94;
P = 0.003), neuro-skeletal (OR = 1.69, 95% CI: 1.22, 2.34;
P = 0.002), and pharyngeal-respiratory (OR = 1.37, 95% CI: 1.07, 1.74;
P = 0.011) somatic complaints for those in the highest tertile of DII compared with those in the lowest tertile. Moreover, after adjustment for stressful life events, medical history, and anti-psychotropic medicines in the fully-adjusted model, the observed associations between DII and all somatic complaints profile remained significant except for pharyngeal-respiratory (OR = 1.23, 95% CI: 0.96, 1.58;
P = 0.102).
Table 4
Crude and multivariable-adjusted odds ratio and 95% confidence interval for the psychosomatic complaints profiles across tertiles of the dietary inflammatory index
n | 939 | 940 | 939 | |
Psychological somatic complaints profile |
Crude | 1 (Reference) | 1.04 (0.86, 1.25) | 1.40 (1.16, 1.69) | < 0.0001 |
Model 1 | 1 (Reference) | 1.16 (0.95, 1.43) | 1.69 (1.34, 2.12) | < 0.0001 |
Model 2 | 1 (Reference) | 1.10 (0.88, 1.37) | 1.65 (1.29, 2.10) | < 0.0001 |
Model 3 | 1 (Reference) | 1.09 (0.87, 1.37) | 1.65 (1.29, 2.12) | < 0.0001 |
Model 4 | 1 (Reference) | 1.05 (0.82, 1.34) | 1.44 (1.10, 1.89) | 0.009 |
Gastrointestinal somatic complaints profile |
Crude | 1 (Reference) | 1.12 (0.91, 1.37) | 1.22 (0.99, 1.49) | 0.058 |
Model 1 | 1 (Reference) | 1.24 (0.99, 1.54) | 1.50 (1.18, 1.92) | 0.001 |
Model 2 | 1 (Reference) | 1.23 (0.97, 1.55) | 1.45 (1.12, 1.88) | 0.005 |
Model 3 | 1 (Reference) | 1.24 (0.98, 1.58) | 1.49 (1.14, 1.94) | 0.003 |
Model 4 | 1 (Reference) | 1.21 (0.94, 1.56) | 1.32 (1.00, 1.75) | 0.048 |
Neuro-skeletal somatic complaints profile |
Crude | 1 (Reference) | 1.00 (0.79, 1.27) | 1.35 (1.06, 1.73) | 0.019 |
Model 1 | 1 (Reference) | 1.08 (0.84, 1.39) | 1.59 (1.18, 2.13) | 0.003 |
Model 2 | 1 (Reference) | 1.19 (0.90, 1.57) | 1.66 (1.21, 2.28) | 0.002 |
Model 3 | 1 (Reference) | 1.20 (0.90, 1.59) | 1.69 (1.22, 2.34) | 0.002 |
Model 4 | 1 (Reference) | 1.23 (0.90, 1.67) | 1.56 (1.10, 2.22) | 0.013 |
Pharyngeal -respiratory somatic complaints profile |
Crude | 1 (Reference) | 1.14 (0.94, 1.38) | 1.22 (1.01, 1.48) | 0.035 |
Model 1 | 1 (Reference) | 1.14 (0.93, 1.39) | 1.29 (1.04, 1.62) | 0.023 |
Model 2 | 1 (Reference) | 1.18 (0.95, 1.46) | 1.32 (1.04, 1.68) | 0.022 |
Model 3 | 1 (Reference) | 1.17 (0.94, 1.46) | 1.37 (1.07, 1.74) | 0.011 |
Model 4 | 1 (Reference) | 1.14 (0.91, 1.43) | 1.23 (0.96, 1.58) | 0.102 |
Means of psychosomatic complaints profiles as well as mean value of DII illustrated significant differences between men and women (Additional file
1: Table S3); indicating sex and DII affect psychosomatic complaints profiles interactively and, therefore, the analyses were separately performed for men and women. Stratified logistic regression analysis demonstrated a sex-specific association between DII and psychosomatic complaints profiles (Table
5). While in the crude model, a greater risk of having higher scores of psychological somatic complaints was observed among men and women in the highest compared with the lowest tertile of DII, these associations tended to be stronger in the adjusted models for men. In contrast, controlling for anti-psychotropic medicines, medical history, and stressful life events was not associated with a significant relation between DII and the psychological somatic complaints of men, whilst it remained significant in all adjusted models for women. The risk of having higher gastrointestinal somatic complaints scores tended to be higher in the highest DII tertile for both men and women, but the significance disappeared in the fully adjusted model for women. In addition, men in the highest tertile DII had a 70% greater risk of having higher scores of pharyngeal-respiratory somatic complaints in the crude model, and the association remained significant even after adjustment for demographic and lifestyle variables, energy, BMI, stressful life event, anti-psychotropic medicine, and medical history (OR = 1.57, 95% CI: 0.03, 2.40;
P = 0.033), whereas no significant association was observed for women. In contrast, a higher DII was significantly associated with increased the risk of higher scores of neuro-skeletal somatic complaints both in crude and adjusted models for women, but not for men.
Table 5
Crude and multivariable-adjusted odds ratio and 95% confidence interval for the psychosomatic complaints profiles across tertiles of the dietary inflammatory index, stratified by sex
Male (n) | 319 | 383 | 452 | |
DII range | −5.55, −2.62 | −2.62, −1.52 | −1.52, 2.62 | |
Psychological somatic complaints profile |
Crude | 1 (Reference) | 1.22 (0.88, 1.68) | 1.46 (1.07, 1.98) | 0.017 |
Model 1 | 1 (Reference) | 1.29 (0.90, 1.84) | 1.50 (1.03, 2.18) | 0.034 |
Model 2 | 1 (Reference) | 1.18 (0.80, 1.73) | 1.41 (0.94, 2.11) | 0.094 |
Model 3 | 1 (Reference) | 1.15 (0.78, 1.70) | 1.43 (0.95, 2.15) | 0.082 |
Model 4 | 1 (Reference) | 1.03 (0.67, 1.59) | 1.16 (0.74, 1.81) | 0.514 |
Gastrointestinal somatic complaints profile |
Crude | 1 (Reference) | 1.17 (0.83, 1.65) | 1.37 (0.99, 1.90) | 0.059 |
Model 1 | 1 (Reference) | 1.32 (0.91, 1.93) | 1.58 (1.07, 2.35) | 0.023 |
Model 2 | 1 (Reference) | 1.34 (0.89, 2.01) | 1.61 (1.05, 2.47) | 0.030 |
Model 3 | 1 (Reference) | 1.37 (0.91, 2.07) | 1.70 (1.10, 2.63) | 0.017 |
Model 4 | 1 (Reference) | 1.36 (0.88, 2.12) | 1.51 (0.94, 2.41) | 0.089 |
Neuro-skeletal somatic complaints profile |
Crude | 1 (Reference) | 1.04 (0.37, 2.91) | 1.42 (0.52, 3.88) | 0.481 |
Model 1 | 1 (Reference) | 1.52 (0.37, 6.15) | 0.72 (0.11, 4.49) | 0.919 |
Model 2 | 1 (Reference) | 1.41 (0.29, 6.99) | 0.83 (0.10, 6.91) | 0.959 |
Model 3 | 1 (Reference) | 1.35 (0.24, 7.73) | 0.84 (0.09, 7.74) | 0.953 |
Model 4 | 1 (Reference) | 7.03 (0.45, 110.1) | 0.48 (0.03, 8.56) | 0.902 |
Pharyngeal -respiratory somatic complaints profile |
Crude | 1 (Reference) | 1.29 (0.94, 1.77) | 1.70 (1.25, 2.30) | 0.001 |
Model 1 | 1 (Reference) | 1.28 (0.90, 1.83) | 1.68 (1.17, 2.43) | 0.005 |
Model 2 | 1 (Reference) | 1.28 (0.87, 1.88) | 1.69 (1.13, 2.51) | 0.009 |
Model 3 | 1 (Reference) | 1.26 (0.86, 1.86) | 1.76 (1.18, 2.64) | 0.005 |
Model 4 | 1 (Reference) | 1.19 (0.80, 1.79) | 1.57 (1.03, 2.40) | 0.033 |
Female (n) | 620 | 557 | 487 | |
DII range | −5.17, −2.61 | −2.61, −1.52 | −1.52, 4.61 | |
Psychological somatic complaints profile |
Crude | 1 (Reference) | 1.02 (0.81, 1.30) | 1.73 (1.34, 2.23) | < 0.0001 |
Model 1 | 1 (Reference) | 1.09 (0.85, 1.40) | 1.87 (1.40, 2.51) | < 0.0001 |
Model 2 | 1 (Reference) | 1.05 (0.80, 1.38) | 1.82 (1.33, 2.49) | < 0.0001 |
Model 3 | 1 (Reference) | 1.05 (0.80, 1.39) | 1.79 (1.30, 2.46) | 0.001 |
Model 4 | 1 (Reference) | 1.04 (0.77, 1.40) | 1.65 (1.16, 2.34) | 0.008 |
Gastrointestinal somatic complaints profile |
Crude | 1 (Reference) | 1.14 (0.88, 1.47) | 1.27 (0.97, 1.66) | 0.076 |
Model 1 | 1 (Reference) | 1.18 (0.90, 1.56) | 1.47 (1.08, 2.02) | 0.016 |
Model 2 | 1 (Reference) | 1.16 (0.87, 1.56) | 1.37 (0.98, 1.90) | 0.065 |
Model 3 | 1 (Reference) | 1.17 (0.87, 1.57) | 1.38 (0.98, 1.93) | 0.063 |
Model 4 | 1 (Reference) | 1.14 (0.83, 1.56) | 1.26 (0.88, 1.80) | 0.205 |
Neuro-skeletal complaints profile |
Crude | 1 (Reference) | 1.01 (0.79, 1.30) | 1.39 (1.08, 1.79) | 0.015 |
Model 1 | 1 (Reference) | 1.07 (0.82, 1.38) | 1.61 (1.19, 2.17) | 0.003 |
Model 2 | 1 (Reference) | 1.18 (0.89, 1.57) | 1.66 (1.20, 2.30) | 0.002 |
Model 3 | 1 (Reference) | 1.20 (0.90, 1.59) | 1.69 (1.21, 2.36) | 0.002 |
Model 4 | 1 (Reference) | 1.21 (0.89, 1.65) | 1.58 (1.10, 2.25) | 0.013 |
Pharyngeal -respiratory somatic complaints profile |
Crude | 1 (Reference) | 1.12 (0.88, 1.41) | 1.05 (0.82, 1.34) | 0.665 |
Model 1 | 1 (Reference) | 1.08 (0.84, 1.38) | 1.10 (0.83, 1.46) | 0.492 |
Model 2 | 1 (Reference) | 1.14 (0.88, 1.49) | 1.14 (0.84, 1.54) | 0.361 |
Model 3 | 1 (Reference) | 1.15 (0.87, 1.50) | 1.18 (0.86, 1.60) | 0.278 |
Model 4 | 1 (Reference) | 1.14 (0.87, 1.51) | 1.09 (0.79, 1.49) | 0.555 |
Discussion
To the best of our knowledge, this is the first study examining the association between the dietary inflammatory index and psychosomatic complaints in an adult population. This study suggests a direct link between a pro-inflammatory diet and various psychosomatic complaints profiles, including psychological, gastrointestinal, neuro-skeletal, and pharyngeal-respiratory somatic complaints, in crude and various adjusted models.
Psychosomatic symptoms are attributed to intracellular inflammation, oxidative stress damage, and gut-derived inflammation [
6]. Higher levels of nuclear factor kappa beta (NF-κβ) is correlated with psychosomatic symptoms, such as muscular tension, fatigue, pain, sadness, and irritability [
6]. Furthermore, increased production of NFκβ, a characteristic of psychological disorders [
42‐
44], stimulates the inflammation pathways through transcriptional activation of inflammatory markers, such as interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) [
6]. Over the last few decades, robust evidence has been accumulated to indicate that elevated inflammatory mediators are a consistent feature of psychiatric diseases [
45], and a meta-analysis has suggested a bidirectional link between systematic inflammation and mental disorders [
46]. Therefore, developing approaches that target inflammatory pathways are warranted to reduce the incidence of mental disorders and psychosomatic complaints.
To date, many studies have examined the effects of diet composition on serum levels of inflammatory markers [
47]. For example, a high glycemic index diet increases NF-κβ activation [
48] and stimulates the inflammatory signaling cascade, whilst whole grains [
49] and a vegetarian diet [
50] may have anti-inflammatory effects. In addition, increased total flavonoid consumption is inversely correlated with serum levels of CRP [
51], which have been attributed to an inhibitory effect on the release of cytokines or down-regulation of pro-inflammatory transcriptional factors [
52]. Taken together, a number of dietary components have been related to pro- or anti-inflammatory pathways and the circulating concentrations of pro- or anti-inflammatory mediators. Despite this, it has been suggested that taking into account diet as a whole, rather than its individual components, may be important, because of the role of potential interactions between, and/or synergistic effects of food components.
In this regard, the DII has been developed as an index reflecting the inflammatory potential of the whole diet. Correlations between the DII with circulating levels of inflammatory mediators have been found in some [
11‐
13], but not all studies [
13,
20]. However, most studies assessing the relation between DII and mental disorders have reported a positive link. In several observational studies, including our own research in this study population, higher DII scores were associated with increased risk of depression or anxiety, or lower likelihood of well-being [
15‐
23]. Due to the close relation between mental disorders and psychosomatic symptoms, an association between DII and psychosomatic complaints is conceivable, and it is expected that amelioration of psychological disorders would improve somatic complaints. However, it is not clear which inflammatory mediators, and to which extent, contribute to developing mental disorders or their somatic symptoms. In the Whitehall II study, despite a significant link between DII and inflammatory biomarkers at baseline, the recurrence of depressive symptoms was not related to the serum concentrations of IL-6 and CRP after a 5-year follow-up [
16]. These findings may suggest that diet-related inflammatory effects are mediated via mediators other than IL-6 and CRP. Moreover, since CRP and IL-6 levels are affected by many modifying factors, such as age, adiposity, physical fitness, and activity, they are unlikely to be specific indicators for systematic inflammation per se [
53]. Thus, further research investigating the link between DII and inflammatory mediators is required.
Furthermore, in studies investigating DII, the inflammatory potential of diet has consistently been associated with a less healthy nutritional profile [
15,
23]. In addition, like a diet with lower potential for inflammation, healthy dietary patterns such as the Mediterranean eating style, healthy eating index, and other healthy patterns identified by posteriori method have been associated with lower serum levels of inflammatory mediators [
54,
55]. Hence, in agreement with our previous work [
24], the results of the present study confirm lower risk of different psychosomatic complaints profiles among individuals with a healthier dietary pattern, and conversely higher risk of psychosomatic complaints profiles among individuals with a Western dietary pattern, which have been assumed to have anti-inflammatory and pro-inflammatory properties, respectively [
24].
Our results revealed that individuals in the lowest tertile of DII were more likely to have a healthier lifestyle (more physical activity and less smoking), be female, and overweight, in spite of having lower energy intakes. The latter finding might be due to underreporting, which is more common in female and overweight/obese subjects [
56], or reverse causality, wherein overweight/obese individuals tend to change their lifestyle and adhere to a healthy diet. Therefore, we further assessed the association between DII and psychosomatic complaints profiles stratified by BMI and found no statistically significant association between any of the psychosomatic complaint profiles and DII in overweight/obese subjects, whereas in subjects with normal weight, a greater DII was associated with increased risk of psychological and neuro-skeletal somatic complaints and tended to increase the risk of gastrointestinal somatic complaints (data not shown). However, in the present study, we are not able to draw any conclusions relating to causality, and longitudinal studies are needed.
This study has some limitations. First, the cross-sectional design did not allow us to investigate cause-effect relationships. For example, it is not clear whether psychosomatic complaints precede adherence to a pro-inflammatory diet, or whether the inflammatory potential of the diet causes psychosomatic complaints. On the other hand, it is possible that individuals who suffer from psychosomatic complaints tend to consume healthier foods with more anti-inflammatory properties to alleviate their symptoms. Second, in the present study, only gastrointestinal symptoms were evaluated using adequate clinical and technical approaches to provide a medical explanation, whilst other somatic symptoms are only indicative of somatization. Third, the DII has not been validated as a proxy measure of the inflammatory potential of diet in our study population; however, the consistency of our findings with others in the context of mental disorders [
23] may confirm its validity. Fourth, the sex-specific association between DII and psychosomatic complaints profiles needs more research to determine the potential modifying effect of sex. It is not clear at this stage whether the different associations are real or attributable to methodological limitations. However, it is possible that some differences in lifestyle factors between men and women, such as smoking habits or physical activity, may explain the sex differences in DII-psychosomatic complaints. Although the confounding effects of such variables have been taken into account, the residual effects of such confounders or unknown or unmeasured confounders may influence the results. Fifth, the population of the study may have the possibility of selection because we selected participants from the working population, such as workers on the university campus and in hospitals and health centers, but not from the general community-dwelling population. Additionally, the subjects included in the study were 2828 of 10,087 subjects (approximately participation rate, 28%); therefore, despite including people with various socioeconomic status, our findings might not be generalizable to other populations. Finally, our study relied on the use of self-reported data.
The strengths of this study include the novelty of the topic and the use of validated questionnaires to evaluate dietary intakes and psychosomatic complaints. In addition, although the study was conducted among university employees, the large sample size of the study population with wide variation in demographic variables may make our results generalizable to other populations.
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