Vitamin B12 (cobalamin) plays a crucial role in neurodevelopment, particularly during pregnancy and early childhood. It is essential for DNA synthesis, red blood cell formation, and nervous system function. Maternal B12 levels are particularly important, as they influence fetal brain development. Inadequate maternal intake during pregnancy may lead to altered neurodevelopmental trajectories and increase the risk of ASD. Postnatally, insufficient dietary cobalamin in infants and young children could further contribute to cognitive and behavioral impairments. One potential mechanism linking low B12 levels to ASD involves its role in the gut microbiota balance. Dysbiosis, commonly observed in individuals with ASD, is associated with increased gut permeability, low-grade inflammation, and disruptions in the gut–brain axis, all of which may contribute to ASD symptoms. Additionally, B12 is essential for neurotransmitter metabolism, particularly in the synthesis of serotonin and dopamine, which regulate mood, cognition, and behavior. Cobalamin also plays a key role in neuronal myelination, which ensures efficient signal transmission in the nervous system. Disruptions in these processes could underlie some of the cognitive and behavioral features associated with ASD. Despite growing evidence, the link between B12 and ASD remains inconclusive due to inconsistent findings across studies. Research suggests that B12 levels may serve as a potential biomarker for disease progression and treatment response. However, many studies rely on single-time-point measurements, failing to account for individual variability, genetic predispositions, dietary intake, and environmental factors, all of which can influence B12 levels and ASD risk. Further longitudinal studies are needed to clarify this relationship.

The impact of weather on mental illness is widely debated, but the mechanism of this relationship remains unclear. The immunoseasonal theory suggests that in winter, a T-helper 1 (Th1) response predominates, impairing Prefrontal Cortex (PFC) control, which exacerbates symptoms of depression, while after it, in summer, a Th2 response predominates in immunologically prone individuals, activating cortical and mesolimbic centers, which can exacerbate symptoms of psychosis. In this paper, we aim to describe the validity of this theory through a narrative review of data related to weather and immunology in psychiatry. This review extends existing literature by integrating immunological findings with psychiatric seasonality research, offering a mechanistic perspective that links Th1/Th2 shifts to specific symptom exacerbations. Winter Th1 severity may worsen depression and anxiety, while summer Th2 dominance appears to be associated with exacerbations of schizophrenia, mania, impulsivity, and suicide risk. It is possible that the mechanism of Th1 response potentiation and deterioration of PFC function is common to most psychiatric entities and is nonspecific. This suggests that seasonal immune dysregulation may play a broader role in psychiatric disorders than previously recognized, challenging the idea that seasonality impacts only selected conditions. Characteristic dysfunctions within an individual determine further differences in clinical manifestations. The mechanism of Th2 potentiation may not be limited to mania and psychosis but may also be associated with increased impulsivity and suicide risk. If the immunoseasonal theory is confirmed, selected immunological markers could be used not only in the diagnosis of psychiatric exacerbations but also in predicting symptom fluctuations and tailoring treatment strategies. This could enable more personalized interventions, such as seasonally adjusted medication dosing or targeted anti-inflammatory therapies. While this mechanism seems plausible, further research, especially analyzing markers of inflammatory and anti-inflammatory responses, is needed to better understand and confirm it.

Numerous scientific findings indicate that excess adipose tissue, particularly visceral fat, is associated with a chronic inflammatory state manifested by elevated levels of proinflammatory cytokines and an imbalance in the T helper type 1/type 2 (Th1/Th2) response, which carries numerous metabolic consequences. Obesity induces, among other effects, the activation of the kynurenine pathway and a reduction in serotonin synthesis, alterations in adipokine profiles, modifications of the hypothalamic–pituitary–adrenal (HPA) axis, disturbances in fatty acid ratios, oxidative stress, and dysfunction of the gamma-aminobutyric acid (GABA)ergic system. These neuroimmunological and metabolic disturbances, along with obesity-induced neurotransmission abnormalities that may represent a common underlying model of depression, could provide valuable insights into the pathomechanisms of depression, allowing for prediction of disease progression and individualized therapeutic strategies in overweight patients. Furthermore, the analysis of inflammation-associated biomarkers opens up new therapeutic perspectives, suggesting that interventions aimed at reducing inflammation might lead to potential advances in the treatment of depression.

Sensory dysregulation represents a core challenge in autism spectrum disorder (ASD), affecting perception, behavior, and adaptive functioning. The brain’s ability to reorganize, known as neuroplasticity, serves as the basic principle for therapeutic interventions targeting these deficits. Neuroanatomical mechanisms include altered connectivity in the sensory and visual cortices, as well as in the limbic system and amygdala, while imbalances of neurotransmitters, in particular glutamate and gamma-aminobutyric acid (GABA), contribute to atypical sensory processing. Traditional therapies used in sensory integration are based on the principles of neuroplasticity. Increasingly, new treatments use this knowledge, and modern therapies such as neurofeedback, transcranial stimulation, and immersive virtual environments are promising in modulating neuronal circuits. However, further research is needed to optimize interventions and confirm long-term effectiveness. This review discusses the role of neuroplasticity in the etiopathogenesis of sensory integration deficits in autism spectrum disorder. The neuroanatomical and neurotransmitter basis of impaired perception of sensory stimuli is considered, and traditional and recent therapies for sensory integration are discussed.

Vitamin D₃ plays a pivotal role not only in bone health but also in the functioning of the nervous system, particularly in the context of age-related neurodegenerative diseases such as Alzheimer’s disease, multiple sclerosis, and Parkinson’s disease. Vitamin D₃ deficiency has been associated with cognitive decline, heightened inflammation, and shortened leukocyte telomere length, which may contribute to accelerated cellular aging. Therapeutic interventions involving vitamin D₃ have been reported in selected clinical studies and meta-analyses to potentially enhance cognitive function, decrease amyloid β biomarkers, and prolong telomere length, although heterogeneity remains across study designs and populations. Furthermore, vitamin D₃ has been shown to influence the expression of genes implicated in DNA repair and oxidative stress response, including NRF2, OGG1, MYH, and MTH1. This narrative review synthesizes current knowledge on the molecular mechanisms of vitamin D₃ action in the context of neuroprotection and discusses potential directions for future research, including its possible therapeutic applications in neurodegenerative diseases.

Emerging evidence highlights the role of chronic low-grade inflammation and dysregulated cytokines in both obesity and schizophrenia, suggesting overlapping immune system pathways that contribute to cognition and nervous system inflammation. Excess adipose tissue functions as an active endocrine organ, releasing pro-inflammatory mediators that may serve as potential biomarkers, while the use of antipsychotic agents in schizophrenia further modifies cytokine profiles and immune responses. A key knowledge gap lies in understanding how adipose-related inflammation modifies the severity of psychotic symptoms, cognitive deficits, and the efficacy of antipsychotic medications. This review aims to present excess adipose tissue as a potential contributor to the development of SCZ or a modifier of treatment efficacy, emphasizing the role of immune imbalance, inflammatory pathways, and metabolic dysfunction. By synthesizing current findings, we aim to present obesity not only as a frequent comorbidity in schizophrenia but also as a potential driver of neuroinflammation and disease progression. Here, we demonstrate that excess adiposity may perpetuate a vicious cycle linking metabolic dysfunction, immune activation, and psychiatric symptomatology. Situating these findings within a broader context, the review underscores the clinical need for inflammation-informed, individualized management strategies that integrate psychiatric care with metabolic monitoring. Ultimately, clarifying the shared inflammatory pathways of obesity and schizophrenia may open new avenues for biomarker development and targeted interventions.