Impact of High-Fat Diet on Neurobehavioral Disorders

The high-fat diet (HFD) has emerged as a crucial environmental factor influencing mental health across the lifespan. Epidemiological and preclinical studies link prolonged consumption of lipid-rich foods to a spectrum of neurobehavioural disturbances, including depressive and anxiety-like phenotypes, cognitive deficits and altered reward processing. Mechanistic investigations implicate chronic neuroinflammation, dysregulated neurotrophic signalling and disrupted synaptic plasticity as central mediators. Excess dietary fat promotes peripheral and central inflammatory cascades that compromise microglial homeostasis and reduce hippocampal neurogenesis, thereby undermining emotional regulation and memory formation. At the molecular level, transcriptional repressors responsive to metabolic stress diminish expression of key neurotrophic factors, while perturbations of gut–brain axis signalling further exacerbate behavioural vulnerability. Importantly, these effects manifest during sensitive developmental windows, such as adolescence, and may predispose individuals to long‐term psychiatric risk. Global prevalence of Westernised dietary patterns underscores the public health urgency, driving efforts to identify inflammatory biomarkers and to evaluate pharmacological or lifestyle interventions—including anti‐inflammatory agents and dietary modulation—to mitigate HFD‐induced neuropsychological dysfunction.

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Impact of High-Fat Diet on Neurobehavioral Disorders publication trend

The graph below shows the total number of articles in impact of high-fat diet on neurobehavioral disorders across all publications each year (not limited to Nature Index journals).

Technical terms

Neuroinflammation: Inflammatory activation within the central nervous system involving cytokines, microglia and astrocytes that can disrupt neuronal function.

Microglial activation: Transition of brain‐resident immune cells to a reactive state characterised by altered morphology and release of inflammatory mediators.

Hippocampal neurogenesis: Generation and integration of new neurons in the hippocampus, critical for learning, memory and emotional regulation.

C/EBPβ: CCAAT/enhancer binding protein β, a transcription factor activated by metabolic stress that can repress neurotrophic gene expression.

BDNF: Brain‐derived neurotrophic factor, a neurotrophin essential for synaptic plasticity, neuronal survival and cognitive function.

References

1. Central and Peripheral Inflammation: A Common Factor Causing Addictive and Neurological Disorders and Aging-Related Pathologies. International Journal of Molecular Sciences (2023).
2. High-Fat Diet Consumption in Adolescence Induces Emotional Behavior Alterations and Hippocampal Neurogenesis Deficits Accompanied by Excessive Microglial Activation. International Journal of Molecular Sciences (2022).
3. Inflammation-activated C/EBPβ mediates high-fat diet-induced depression-like behaviors in mice. Frontiers in Molecular Neuroscience (2022).