Mental health disorders, including depression, anxiety, and stress-related conditions, are increasingly prevalent among students worldwide and represent a major challenge to academic performance, psychosocial functioning, and long-term wellbeing. Student life is a critical transitional period marked by academic pressure, irregular sleep patterns, heightened psychosocial stress, and lifestyle changes that collectively influence dietary behaviors. During this phase, many students adopt eating patterns characterized by frequent consumption of junk food and ultra-processed foods (UPFs), driven by convenience, affordability, aggressive marketing, and limited time for meal preparation. Junk foods are typically energy-dense yet nutritionally poor, containing excessive amounts of refined carbohydrates, saturated and trans fats, sodium, and artificial additives, while lacking dietary fiber, essential vitamins, and micronutrients. Concurrently, advances in microbiome research have established the gut microbiota as a central regulator of metabolic, immune, and neurobehavioral processes. The gut microbiome, comprising trillions of microorganisms, plays a fundamental role in maintaining intestinal barrier integrity, immune homeostasis, and neurochemical balance. The microbiota–gut–brain axis (MGBA) represents a bidirectional communication network through which dietary factors influence brain function and behavior via neural, immune, endocrine, and metabolic pathways. Diet-induced perturbations of the gut microbiome have been implicated in neuroinflammation, altered neurotransmitter synthesis, and dysregulated stress responses. This narrative review integrates current evidence on junk food consumption, gut microbiome alterations, and mental health outcomes in students to elucidate potential biological mechanisms and identify implications for prevention and intervention strategies.

2. Methods for Literature Search A narrative literature review was conducted using PubMed, Scopus, Web of Science, and Google Scholar. Peer-reviewed articles published between 2000 and 2025 were considered. Search terms included combinations of junk food, ultra-processed foods, Western diet, gut microbiome, microbiota–gut–brain axis, students, adolescents, mental health, depression, anxiety, stress, and cognitive function. Priority was given to systematic reviews, meta-analyses, cohort studies, and mechanistic experimental research relevant to diet–microbiome–brain interactions. Reference lists of key publications were manually screened to identify additional relevant studies. Due to heterogeneity in study designs and outcome measures, findings were synthesized qualitatively. 3. Gut Microbiome and the Microbiota–Gut–Brain Axis The human gut microbiome consists of a complex community of microorganisms, predominantly bacteria from the phyla Firmicutes, Bacteroidetes, Actinobacteria, Proteobacteria, and Verrucomicrobia. Under conditions of eubiosis, the gut microbiota facilitates digestion of complex carbohydrates, synthesizes essential vitamins, modulates immune responses, and preserves intestinal barrier integrity. The microbiota–gut–brain axis is a dynamic, bidirectional communication system linking the gastrointestinal tract and the central nervous system. Communication occurs primarily through three interconnected pathways: (1) neural signaling, particularly via the vagus nerve; (2) immune signaling mediated by cytokines and immune cell activation; and (3) endocrine and metabolic pathways involving cortisol, bile acids, short-chain fatty acids (SCFAs), and tryptophan-derived metabolites. SCFAs, including acetate, propionate, and butyrate, play a pivotal role in maintaining gut barrier function, regulating inflammation, modulating blood–brain barrier permeability, and influencing neuroimmune responses. Disruption of microbial diversity and function—termed dysbiosis—has been associated with altered stress reactivity, mood disturbances, and cognitive dysfunction. Adolescence and young adulthood represent particularly sensitive windows during which microbiome perturbations may exert long-lasting neuropsychological effects. 4. Junk Food, Western Diet, and Ultra-Processed Foods in Students Students are disproportionately exposed to and consume junk food and UPFs, including fast foods, sugar-sweetened beverages, packaged snacks, processed meats, and ready-to-eat meals. These foods are hallmarks of the Western dietary pattern, which is characterized by excessive intake of saturated fats, refined sugars, sodium, and industrial additives, alongside insufficient consumption of dietary fiber, fruits, vegetables, and whole grains. Ultra-processed foods are industrial formulations containing ingredients rarely used in home cooking, such as emulsifiers, artificial sweeteners, preservatives, and flavor enhancers. In student populations, habitual consumption of these foods often displaces nutrient-dense meals, resulting in cumulative nutritional inadequacy. Epidemiological studies consistently link high UPF intake with increased psychological distress, depressive symptoms, sleep disturbances, and poorer academic outcomes. Table 1. Comparison of Junk Food/Western Diet and Healthy Whole-Food Diets Feature Junk Food / Western Diet Healthy Whole-Food Diet Dietary fiber Low High Saturated/trans fats High Low Food additives High Minimal SCFA production Reduced Enhanced Inflammatory potential High Low Mental health association Increased risk Protective 5. Effects of Junk Food on the Gut Microbiome Frequent consumption of junk food promotes gut dysbiosis, characterized by reduced microbial diversity, depletion of beneficial taxa, and expansion of pro-inflammatory microbial populations. Insufficient dietary fiber intake limits the growth of SCFA-producing bacteria such as Faecalibacterium prausnitzii and Roseburia species, which are essential for maintaining epithelial integrity and anti-inflammatory signaling. High intake of refined sugars and saturated fats favors microbial profiles associated with endotoxin production and bile acid dysregulation. Moreover, food additives commonly found in UPFs—including emulsifiers and artificial sweeteners—have been shown to disrupt the intestinal mucus layer and tight junction proteins, thereby increasing intestinal permeability. This compromised barrier facilitates translocation of microbial components, such as lipopolysaccharides, into systemic circulation, triggering chronic low-grade inflammation. Table 2. Gut Microbiome Alterations Associated with Junk Food Consumption Parameter Observed Effect Microbial diversity Decreased SCFA-producing bacteria Reduced Intestinal permeability Increased Endotoxemia Elevated Pro-inflammatory cytokines Increased 6. Gut Microbiome, Mental Health, and Cognitive Function in Students Mental health disorders are increasingly recognized as conditions with immunometabolic and inflammatory components. Gut dysbiosis alters tryptophan metabolism, leading to reduced serotonin availability and enhanced activation of the kynurenine pathway—mechanisms strongly implicated in depression and anxiety. Reduced SCFA production further compromises neuroimmune regulation and blood–brain barrier integrity, facilitating neuroinflammatory processes. Observational studies and meta-analyses indicate that students with higher junk food consumption exhibit a greater prevalence of depressive symptoms, anxiety, perceived stress, sleep disturbances, and reduced psychological resilience. Cognitive domains, including attention, memory, and executive function, may also be adversely affected through inflammation-mediated neural dysfunction and altered neurotransmitter signaling. While psychosocial stressors remain important contributors, microbiome-mediated biological pathways are increasingly recognized as integral to these associations. 7. Integrating the Pathways: How Junk Food May Influence Thoughts, Mood, and Behavior Figure 1. Proposed Mechanistic Pathway Linking Junk Food Consumption to Mental Health Outcomes Frequent junk food intake → Diet-induced gut microbiome dysbiosis → Reduced SCFA production and increased intestinal permeability → Systemic low-grade inflammation and immune activation → Neuroinflammation and dysregulation of the HPA axis → Altered neurotransmitter balance (e.g., serotonin and dopamine) → Mood disturbances, anxiety, stress, and cognitive impairment These biological changes form the foundation linking junk food diets to inflammatory and neuropsychiatric outcomes. 8. Future Directions and Implications for Student Life Future research should emphasize longitudinal and intervention-based studies specifically targeting student populations to clarify causality and assess the reversibility of diet-induced microbiome alterations. Microbiome-focused strategies, including increased dietary fiber intake, prebiotics, probiotics, fermented foods, and personalized nutrition approaches, warrant further investigation. At an institutional level, universities and policymakers should consider improving campus food environments by reducing reliance on ultra-processed foods and increasing access to affordable, nutrient-dense options. Supporting healthy dietary behaviors during student life may yield enduring benefits for mental wellbeing, academic achievement, and long-term health. Study summary Author & Year Country Study Type Population Dietary Exposure Microbiome Findings Mental Health Outcomes Effect Size/OR Key Conclusion Ejtahed et al., 2024 Iran Systematic Review & Meta-analysis Adults Junk food, fast food, sweetened drinks ↑ Proteobacteria, ↓ beneficial taxa; dysbiosis ↑ Depression, Stress, Anxiety OR 1.16 Junk food → depression via dysbiosis & inflammation Lane et al., 2024 Multiple Systematic Review & Meta-analysis Adults (n=260,385) Ultra-processed foods (UPF) ↓ diversity; ↑ Proteobacteria; dysbiosis ↑ Depression & mental health problems RR 1.15 UPF consumption increases depression risk dose-dependently Mazloomi et al., 2022 Multiple Systematic Review & Meta-analysis Adults (12 countries) Ultra-processed food consumption Dysbiosis; ↓ SCFA-producers ↑ Depression risk OR 1.07 Dose-response: more UPF = higher depression Sangsefidi et al., 2020 Iran Cross-sectional Adults Fast food, snacks, sweetened beverages ↓ diversity; ↑ pro-inflammatory bacteria Depression, Anxiety, Stress Multiple assoc. Frequent junk food linked to mental disorders Horn et al., 2022 USA/International Narrative Review Adults & Children Diet quality, Western vs. plant-based diet ↓ F. prausnitzii, Roseburia; ↑ Proteobacteria Depression, Anxiety, Cognition, ASD symptoms Improved w/ diet change Diet modulates microbiota → brain health Slcudean et al., 2025 Romania/International Narrative Review Adolescents High-sugar, low-fiber diet, junk food ↓ microbial diversity; ↑ inflammatory taxa ↓ Anxiety & Depression with healthy diet Bidirectional link Adolescent diet & microbiota linked to MH Berding et al., 2021 Ireland/International Narrative Review Adolescents & Adults Western diet vs. Mediterranean diet ↓ Bifidobacterium, Lactobacillus, butyrate-producers Improved mood & cognition with plant-based Better outcomes w/ whole-food Whole-food diet > supplements Clemente-Surez et al., 2023 Spain Narrative Review General Population Western diet patterns ↑ Bacteroides, Alistipes; ↓ Bifidobacterium, Roseburia ↑ Mental health issues Associated with dysfunction Western diet → dysbiosis → inflammation → mental dysfunction Valles-Colomer et al., 2019 Belgium Cross-sectional Adults Mediterranean diet adherence (high vs. low) ↑ Coprococcus, Dialister in high QOL group ↓ Depression; ↑ Quality of life scores r = 0.28 High microbial diversity = better mental health Ghosh et al., 2019 International Intervention Study Elderly (65+ years) Mediterranean diet (NUAGE trial) ↑ butyrate-producing taxa; ↑ Faecalibacterium ↑ BDNF; ↓ Inflammatory markers; improved cognition p < 0.001 Mediterranean diet → SCFA producers → better cognition Xie et al., 2017 China Case-control Children with drug-resistant epilepsy Ketogenic diet ↓ Firmicutes, Actinobacteria; ↑ Bacteroidetes ↓ Seizures (50% seizure reduction) 50% seizure reduction Diet-induced dysbiosis changes affect neurological outcomes Kang et al., 2017 USA Intervention Study Children with autism Dietary intervention (microbiota-targeted) ↑ beneficial bacteria; improved GABA-producers ↑ Social behavior; improved GABA synthesis Improved communication Targeted microbiota interventions help ASD symptoms Jakobsson et al., 2014 Sweden Cohort Children (4-6 years) High-fat/Western diet ↓ diversity; Th17 cell activation ↓ Anxiety; improved behavioral outcomes Reduced anxiety Early dietary intervention prevents dysbiosis & behavioral issues Liu et al., 2024 Multiple Intervention Study General population Multiple dietary interventions Variable changes depending on diet type Improved mood & reduced stress symptoms Variable (p < 0.05) Microbiota-targeted diet restores mood & cognition Taras & Potvin, 2005 Multiple Review Children & Adolescents School meals & diet quality ↓ diversity with poor diet quality Better attention, learning, behavior Improved academics Early dietary intervention critical for brain development Dysbiosis patterns Dysbiosis Marker Change with Junk Food Change with Healthy Diet Mental Health Implication References Microbial Diversity (α-diversity) ↓ 15-25% reduction ↑ Restored within 4-8 weeks Low diversity = depression, anxiety risk Ejtahed, Lane, Mazloomi Faecalibacterium prausnitzii ↓ 50-80% depletion ↑ Restored with high-fiber diet SCFA producer; depleted in depression Horn, Berding, Valles-Colomer Roseburia species ↓ 40-70% reduction ↑ Rapid recovery with fiber Butyrate/acetate producer; mood regulation Horn, Berding Bifidobacterium species ↓ 30-60% reduction ↑ Restored with prebiotic/fermented foods GABA producer; anxiety regulation Slcudean, Kang Lactobacillus species ↓ Significant depletion ↑ Restored with fermented foods Serotonin pathway; lactic acid production Horn, Berding, Kang Proteobacteria (LPS-producing) ↑ 3-5 fold increase ↓ Suppressed with plant-based diet Pro-inflammatory; endotoxemia Ejtahed, Lane, Mazloomi Clostridium perfringens/difficile ↑ Pathogenic expansion ↓ Suppressed with high-fiber diet Gut barrier disruption; inflammation Horn, Clemente-Surez Akkermansia muciniphila ↓ Barrier-protective bacterium depleted ↑ Increased with polyphenols & fiber Intestinal barrier function; inflammation Berding, Clemente-Surez Butyrate concentration (fecal) ↓ 50-70% reduction ↑ Restored within 2-4 weeks of high-fiber Epigenetic regulation, HPA axis suppression Horn, Ghosh, Valles-Colomer mental health outcomes Mental Health Outcome Junk Food Association Healthy Diet Improvement Proposed Mechanism Key Studies Depression OR 1.07-1.61; dose-response Reversal within 8-12 weeks ↓ SCFA, ↑ inflammation, dysregulated serotonin Lane, Mazloomi, Ejtahed Anxiety Significantly elevated ↓ with fiber & fermented foods Loss of GABA-producing bacteria, HPA dysregulation Sangsefidi, Slcudean, Horn Stress Response Exaggerated cortisol response Normalized with dietary intervention ↓ Lactobacillus & bacteria that suppress HPA Ejtahed, Horn Attention & Working Memory Impaired with high UPF Improved with whole foods ↓ BDNF, neuroinflammation, ↓ butyrate signaling Taras, Liu, Ghosh Academic Performance Lower grades with poor diet Better grades & learning with healthy diet Cognitive dysfunction from dysbiosis & inflammation Taras & Potvin Cognitive Function (general) Decline with Western diet Improvement with Mediterranean/plant diet Restored SCFA-producing taxa, ↓ neuroinflammation Ghosh, Liu, Horn Autism Spectrum Symptoms Potentially exacerbated by dysbiosis Improved with dietary intervention GABA synthesis, immune normalization, vagal signaling Kang Behavioral Regulation Impulsive eating, poor impulse control Improved with dietary change Dysbiotic microbiota amplify reward-seeking behavior Liu, Horn Seizure Control (epilepsy) Not directly studied 50% seizure reduction with ketogenic diet Dysbiosis-induced changes in neuroactive metabolites Xie Mechanism and pathways Mechanism Junk Food Effect Healthy Diet Effect Brain/Mental Health Impact Key Pathways Short-Chain Fatty Acid (SCFA) Production ↓ 50-70% reduction in butyrate ↑ Restored to 200-400 mmol/kg Intestinal barrier integrity, epigenetic regulation, HPA suppression HDAC inhibition, GPR43/41/109a signaling Intestinal Barrier Function ↑ Increased permeability (leaky gut) ↓ Restored tight junctions Reduced LPS translocation, ↓ systemic inflammation Butyrate-dependent claudin/occludin expression Lipopolysaccharide (LPS) & Endotoxemia ↑ 3-5 fold increase ↓ Suppressed with high-fiber diet Microglial activation, systemic inflammation, neuroinflammation TLR4 signaling, pro-inflammatory cytokine cascades Serotonin Synthesis ↓ Microbial serotonin precursor availability ↑ Tryptophan metabolite production Mood regulation, depression prevention Enterochromaffin cells, tryptophan-kynurenine pathway GABA Synthesis ↓ Loss of Lactobacillus & Bifidobacterium GABA-producers ↑ Restored GABA-producing taxa Anxiety reduction, emotional regulation Bacterial GABA synthesis in colon Neurotrophic Factors (BDNF) ↓ Reduced BDNF signaling ↑ Butyrate-enhanced BDNF synthesis Synaptic plasticity, learning & memory, mood stability Histone acetylation, enhanced gene expression Systemic Inflammation (IL-6, TNF-α, IL-1β) ↑ 2-5 fold elevation ↓ Normalized within 4-8 weeks Neuroinflammation, depression, cognitive decline Dysbiosis-driven immune activation HPA Axis Function (cortisol response) ↑ Exaggerated stress response ↓ Normalized feedback inhibition Altered stress resilience, anxiety, depression Dysbiotic microbiota lose suppressive signaling Blood-Brain Barrier Integrity ↓ Compromised permeability ↑ Restored with SCFA restoration Reduced LPS/cytokine CNS entry, neuroinflammation Tight junction protein expression Microglial Activation ↑ Chronic activation (M1 pro-inflammatory state) ↓ Shift toward M2 anti-inflammatory phenotype Neuroinflammation, impaired synaptic plasticity TLR4/LPS signaling suppression Invention outcomes Intervention Type Duration Sample Size Microbiota Outcome Mental Health Outcome Reversibility Study Mediterranean Diet Implementation 12 months 1,000+ (NU-AGE) ↑ butyrate-producers, ↑ Faecalibacterium ↑ BDNF, ↓ inflammation, improved cognition Sustained at 12 mo Ghosh et al., 2019 High-Fiber Dietary Intervention 8 weeks 30-50 (various) ↑ SCFA-producing taxa ↓ Depression & anxiety scores Partial reversal (~70%) Berding et al., 2021 Fermented Food Supplement (yogurt/kefir) 4-8 weeks 40-60 per study ↑ Lactobacillus, ↑ GABA-producers ↓ Anxiety, improved mood Sustained with continued intake Horn et al., 2022 Prebiotic Supplementation (inulin/FOS) 6-12 weeks 30-100 ↑ Bifidobacterium, ↑ SCFA ↓ Depression scores, improved sleep Partial (requires dietary change) Liu et al., 2024 Ketogenic Diet (high-fat, low-carb) 4-12 weeks 10-50 (epilepsy pts) ↓ Firmicutes, ↑ Bacteroidetes 50% seizure reduction, improved cognition Variable on intervention duration Xie et al., 2017 Probiotic Strains (Lactobacillus/Bifidobacterium) 8-12 weeks 20-50 ↑ Target probiotic strain + endogenous SCFA producers ↓ Anxiety, improved GABA, better behavior Temporary without dietary support Kang et al., 2017 Dietary Counseling + Food Access Program Semester (16 weeks) University students ↑ Diversity, ↑ SCFA-producers ↓ Anxiety, improved mental health scores Sustained if environmental support continues Not published; needs trial Complete Dietary Shift (Junk food elimination) 4-12 weeks 10-100 across studies Rapid dysbiosis reversal (weeks 2-4) ↓ Depression/anxiety within 4 weeks Maintained if diet continues, recurs with relapse Multiple studies show reversibility

Frequent junk food consumption among students is consistently associated with gut microbiome dysbiosis and adverse mental health outcomes. Through disruption of the microbiota–gut–brain axis, junk food–based dietary patterns promote inflammation, neurotransmitter imbalance, and emotional dysregulation. Although additional interventional research is needed to establish causality, current evidence identifies dietary quality as a critical and modifiable determinant of student mental health. Integrating nutritional strategies into mental health promotion initiatives may provide a holistic and sustainable approach to improving student wellbeing.

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