Obesity, defined as excess body weight for a given height, is a crucial global problem with life-threatening consequences. The associated excess adiposity evolves slowly, with long-term-positive energy balance. There is apoptosis of adipocytes, leading to tissue remodelling and eventual high number of macrophages — all this leading to a low-grade systemic inflammatory state [10,11,12].
Obese individuals tend to be at higher risk of developing not only diseases like type 2 diabetes mellitus, fatty liver disease and cardiovascular diseases but also various otorhinolaryngological diseases like otitis media with effusion, rhinosinusitis and allergy, laryngopharyngeal reflux disease and post/peri complications of adenostonsillectomy [13].
The mean age of presentation in our study was 40.66 ± 7.25 years, there being no statistically significant difference between each of the experimental group (groups A, B, C, D, E) and control group (group F) being statistically insignificant (p-value = 0.65). This observation was consistent with study conducted by Kim T. H. et al. (2015) [14]. Male to female ratio was 1:1.6 in our study; there was female preponderance in all groups, with the difference between each of the experimental group (groups A, B, C, D, E) and control group (group F) being statistically insignificant (p-value = 0.34). This observation was consistent with study conducted by Nam J. S. et al. (2021) [15]; however, Ahmed S. et al. (2014) [16] showed male preponderance in their study. The difference in gender distribution from previous studies could be due to variation in demographic distribution from one population to other.
The percentage of obese patients in group F was 20.5% (23 patients). The percentage of obese patients was 53.6% (51 patients) in group A, 49.7% (85 patients) in group B, 39.5% (17 patients) in group C, 54.9% (56 patients) in group D and 31.3% (21 patients) in group E. Upon comparison with group F, the difference in percentage of obese patients was statistically significant in each of the experimental group (group A: p = 0.0001, group B: p = 0.0001, group C: p = 0.0029, group D: p = 0.001 and group E: p = 0.034). Obese patients were more likely to have otitis media with effusion (OR 1.85, 95% CI 0.15 to 6.49), chronic otitis media (OR 1.80, 95% CI 0.15 to 6.33), sudden SNHL (OR 1.62, 95% CI 0.21 to 6.40), chronic rhinosinusitis (OR 2.05, 95% CI 0.15 to 6.55) and chronic tonsillitis (OR 1.60, 95% CI 0.16–6.13), than the control group.
Also, in our study, as the severity of disease increased with increase in severity of BMI, showing positive correlation for all study groups. As per WHO Asia–Pacific BMI value, in OME group (n = 95), the average hearing impairment in OME group as per BMI was 28.5 dB in obese patients (n = 51), 26 dB in overweight (n = 32), 22.5 dB in normal (n = 8) and 22 db in underweight patients (n = 4), showing positive correlation between severity of OME and severity in grading of BMI (Pearson correlation coefficient = 0.77). In COM group (n = 171), average hearing impairment was 41.5 dB in obese (n = 85), 35 dB in overweight (n = 61), 32.5 dB in normal (n = 11) and 31 dB in underweight (n = 14), showing positive correlation between severity of CRS and BMI (Pearson correlation coefficient = 0.90). In sudden SNHL group (n = 43), average hearing impairment was 44 dB in obese (n = 17), 40 dB in overweight (n = 15), 38.5 dB in normal (n = 6) and 38 dB in underweight (n = 5), showing positive correlation between severity of CRS and BMI (Pearson correlation coefficient = 0.49).
In CRS group (n = 102), mean Adelaide score was 22.31 in obese patients (n = 56), 22.1 in overweight patients (n = 26), 17.5 in normal (n = 14) and 17.2 in underweight (n = 6), showing positive correlation between severity of CRS and BMI (Pearson correlation coefficient = 0.83). In chronic tonsillitis group (n = 67), majority of patients (81.2%) in obese category (n = 21) had grade 4 tonsil size, majority (79.4%) of overweight patients (n = 17) had grade 3 tonsil size, majority of patients (78.1%) having normal BMI (n = 15) had grade 2 tonsil size and majority of patients having (77.9%) underweight BMI (n = 14) had grade 2 tonsil size, showing positive correlation between severity of CRS and BMI (Pearson correlation coefficient = 0.10).
Now, upon considering each case group individually, we try to explain our study findings. It was found that the mean BMI in group of patients with otitis media with effusion (group A) was 25.44 ± 2.81 kg/m2, which was significantly higher than control group (mean BMI = 22.51 ± 3.01 kg/m2). This was consistent with studies conducted by Kaya S. et al. (2017) [17] and Choi H. G. et al. (2015) [18]. Obesity is characterised by higher concentrations of inflammatory mediators such as IL-6 and TNF alpha, and some studies have shown the presence of both these mediators in middle ear fluid of OME patients [19]. Besides this known association between OME and obesity, we in our study also found that out of 95 patients with OME, 42 patients (44.2%) had associated features suggestive of allergic rhinitis, and 11 patients (11.5%) gave associated history of GERD. Obesity leads to reduced adiponectin levels, which downregulates T cells, leading to altered host immunity and allergy. Allergic rhinitis induces mast cells in nasal mucosa to secrete various inflammatory mediators, resulting in Eustachian tube occlusion and OME [20]. Huang S. L. et al. (1999) [21] also showed in their cross-sectional study that BMI was a significant predictor of allergic rhinitis and OME. However, Sybilski D. et al. (2015) [22] could not find any correlation between obesity and allergic rhinitis. In addition, the reason for GERD in obese individuals of our study could be due to increased intragastric pressure and/or lower oesophageal sphincter incompetence. Thus, obesity led to GERD, which then by way of gastric reflux reaching middle ear through nasopharynx and Eustachian tube resulted in OME [23]. Rodrigues M. M. et al. (2014) [24] also suggested in their study that GERD and obesity are positively correlated.
In our study, the mean BMI was 25.12 ± 2.34 kg/m2 in group B (chronic otitis media), the difference between group B and control group being statistically significant (p = 0.0021). Similar finding was shown by Kim T. H. et al. (2015) [14]. Obesity-associated low-grade inflammation leads to the expression of cytokines (like IL-6, TNF alpha, fibroblast growth factor and bone morphologenetic proteins) involved in the pathogenesis of chronic otitis media, resulting in tissue remodelling and inflammatory cell proliferation [25].
In our study, the mean BMI was 25.78 ± 3.14 kg/m2 in sudden SNHL group (Table 2), the difference of mean BMI between this group and control group being statistically significant (p = 0.0001). Lee J. S. et al. (2015) [26] and Lalwani et al. (2013) [27] also in their study showed that increased BMI is significantly associated with prevalence of sudden SNHL. However, Hwang J. H. et al. (2015) [28] stated that there was no association between BMI and sudden SNHL. The reason for association between obesity and sudden SNHL could be due to obesity-associated microangiopathy in the vascular supply of cochlea, leading to pathological damage to inner ear [29]. In our study, out of 43 patients with sudden SNHL, 17 patients had hyperlipidaemia. The reason for sudden SNHL in these patients could be due to atherosclerosis in cochlear microvasculature due to elevated blood lipid levels.
In addition, the mean BMI of chronic rhinosinusitis group was 25.78 ± 2.33 kg/m2 which was significantly higher than mean BMI of control group. Bhattacharya N. et al. (2013) [30] and Chung S. D. et al. (2014) [31] also in their study showed increased association between chronic rhinosinusitis and obesity. The reason for association between obesity and chronic rhinosinusitis could be due to the changes in expression of obesity-linked cytokines, these cytokines being associated with chronic rhinosinusitis as well [32]. Besides this reason, in our study, we also found that 33 obese patients (32.3%) out of total 102 patients of group D with chronic rhinosinusitis also gave clinical history of GERD. Loehrl et al. (2012) [33] also suggested association between GERD and chronic rhinosinusitis. The reason could be due to impaired mucociliary clearance due to direct exposure of nasal mucosa to gastric acid [34]. However, there is very limited data support of this and needs further survey as both GERD and CRS are very commonly prevalent conditions, which could occur independently in a person as well.
In our study, the mean BMI was 25.03 ± 1.84 kg/m2 in group E (chronic tonsillitis), the difference between group E and control group (group F) being statistically significant (p = 0.004). This finding was consistent with observations made by Kim T. H. et al. (2015) [14] and Narang I. et al. (2012) [35]. Besides the known reason of obesity-associated cytokine expression, another reason for this could be mouth-breathing tendency among obese people and obesity-associated endocrine-mediated somatic growth, thus predisposing to recurrent larger tonsils.