There is a dearth of evidence on the association between dietary patterns and pterygium. In this study, we identified three dietary patterns—healthy diet, protein, and carbohydrate patterns. The score for healthy dietary patterns, which included a high intake of green and yellow vegetables, other vegetables, potatoes, fruits, and fish and shellfish, was associated with a low risk for pterygium. In addition, the intake of retinol equivalents (vitamin A) was inversely related to the risk of pterygium. To our knowledge, this is the first study to evaluate the association of pterygium with dietary patterns and nutrient intake.
The relationship between pterygium and vitamin D was reported in a previous study [21] that was based on the consideration that UV exposure is a major risk factor for developing pterygium and that vitamin D production is primarily influenced by UV exposure. However, despite its anti-neovascular and anti-inflammatory properties, vitamin D is ineffective in protecting the conjunctiva from the harmful effects of UV rays.
One important aspect of salutogenesis is healthy eating, which has no precise definition. Nevertheless, the concept of healthy eating is generally based on a nutritionally balanced diet of natural/unprocessed foods and low amounts of fat [22]. Studies suggest that self-assessed healthy eating behavior comprises judging the macronutrient composition of a meal and adhering to dietary guidelines that recommend decreased levels of fat, sugar, and salt as well as increased levels of vegetables and fruits [23]. These diets, along with the consistent influence of antioxidant activity, protect against major age-related eye diseases, such as AMD [24], cataracts [25], glaucoma [26], and diabetic retinopathy [27]. Our study suggests that pterygium may also be included in this list.
In general, vegetables contain high levels of vitamins, minerals, and dietary fiber, which can be efficiently provided by healthy dietary habits. In this study, retinol equivalents (vitamin A), one of the most abundant vitamins in vegetables, were associated with pterygium. Vitamin A functions mostly through nuclear retinoic acid, retinoid X, and peroxisome proliferator-activated receptors. Retinoids regulate the growth and differentiation of many cell types within the skin, and their deficiency leads to abnormal epithelial keratinization. One well-established example is the Bitot spot, a conjunctival lesion classically associated with severe vitamin A deficiency [28]. The critical factor for the initiation of pterygium is limbal reorganization through the formation of pterygium cells, rather than through simple limbal failure. This reorganization is thought to be associated with UV-induced damage or genetic susceptibility [29]. Apart from pterygium cells, the cytology of superficial cells in such lesions has revealed a unique feature at the surface—squamous metaplasia associated with an increased population of goblet cells [30]. Squamous metaplasia is the consequence of various ocular surface conditions, including dry eye syndrome and vitamin A deficiency [31]. In wounded tissues, vitamin A stimulates epidermal turnover, increases the rate of re-epithelialization, and restores the epithelial structure, all of which can be expected to reduce the migration of pterygium cells.
Neovascularization plays a major role in the proliferation of pterygium and may promote the transformation of pterygium from the quiescent stage to the progressive stage [32]. Dong et al. reported significantly higher levels of vascular endothelial growth factor (VEGF) protein expression in pterygium tissues than in the normal conjunctiva [33]. VEGF is a specific heparin-binding growth factor that acts through receptors on vascular endothelial cells to promote proliferation and migration, thus stimulating angiogenesis [34]. Conversely, retinoids have several similar biological activities, such as antioxidant properties, inhibition of malignant tumor growth, and induction of apoptosis [35]. These findings suggest that retinoids may contribute to the inverse correlation between vitamin A and pterygium risk via their antioxidant properties, thereby exerting a protective effect.
Our study has some limitations. First, the causal relationship between dietary patterns and pterygium could not be investigated owing to the study design. Longitudinal dietary data are required to confirm this relationship. Second, dietary, exercise, and smoking behaviors were determined using self-reported questionnaires, which could have been influenced by the participants’ biases, including under- and over-reporting. Although this is a limitation of the study design, it is desirable to use objective indicators whenever possible. Third, we only used data on physical activity during leisure time; the participants’ physical activity during work was unclear. Finally, the site, size, and degree of pterygium invasiveness were not evaluated. Despite these limitations, our study is valuable. To our knowledge, this is the first study to investigate the impact of dietary patterns on the risk of pterygium. Further studies are required to confirm our findings.