Candidiasis – Causes, Symptoms, Treatment, Antifungal Diet

The principal mechanism facilitating colonization and pathogenic overgrowth of *Candida* species fungi is immune system dysfunction, precipitated by both chronic metabolic disorders (e.g., hyperglycemia in type 1 and type 2 diabetes mellitus) and secondary immunosuppressed states—including HIV infection, glucocorticoid therapy, or biologically modified immune response inhibitors. Iatrogenic factors play a similarly critical role, particularly broad-spectrum antibiotics, which—by eradicating competitive bacterial flora in the gut and mucosal surfaces—create an ecological niche for opportunistic microorganisms. Hormonal imbalances (e.g., elevated estrogen levels during pregnancy, fluctuations in the perimenopausal period) and exogenous administration of synthetic hormones (oral contraceptives, hormone replacement therapy) alter local microenvironmental conditions, thereby facilitating fungal cell adhesion and invasion. Additionally, disturbances in carbohydrate metabolism—both congenital (e.g., glucose transporter defects) and acquired (insulin resistance)—generate elevated concentrations of energetic substrates in bodily fluids, providing an optimal medium for the proliferation of *Candida albicans* and related species. A diet deficient in prebiotics and polyphenols but rich in high-glycemic-index simple sugars, fermented alcohols, and ultra-processed foods exacerbates intestinal dysbiosis and systemic inflammatory responses, cumulatively increasing susceptibility to fungal infections. Behavioral factors, such as chronic oxidative stress (linked to insufficient regenerative sleep or excessive psychological burden), tobacco smoking (particularly in the context of oral candidiasis among poorly fitted or inadequately cleaned denture wearers), and wearing non-breathable synthetic clothing (e.g., polyester), promote localized moisture retention and elevated skin temperature, predisposing individuals to dermatological and mucosal infections. Epidemiological research (including Rodrigues et al., 2019; Bouopda Tamo, 2020) confirms that the interplay of these endogenous and exogenous determinants governs both the prevalence and clinical severity of candidiasis.