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2025-08-14

Schizophrenia: when sugar plays with the brain

Psychiatry

By Ana Espino | Published on August 14, 2025 | 2 min read


#Schizophrenia #CognitiveFunction #MetabolicDisorder  


Schizophrenia is a severe psychiatric disorder characterized by psychotic symptoms, cognitive impairments, and global disruption of social and occupational functioning. Among its many associated comorbidities, metabolic disorders—particularly impaired glucose regulation—play a central role. These abnormalities, often present from the earliest stages of the illness, are linked both to the effects of antipsychotic treatment and to pathophysiological factors inherent to schizophrenia.  

Current treatments mainly target psychotic symptoms, but their impact on metabolic disturbances and cognitive functions remains limited. Cognitive deficits are among the main determinants of functional disability and may be exacerbated by abnormalities in glucose homeostasis. A major challenge is therefore to better understand the relationship between glucose regulation and cognitive performance in schizophrenia, in order to identify potential therapeutic targets and improve overall patient care.  

In this context, this study set out to evaluate the association between metabolic parameters (blood glucose, insulin, HOMA-IR) and cognitive performance across different domains in patients with schizophrenia.    


What if blood sugar dictated our thoughts?  


A total of 175 patients diagnosed with schizophrenia were assessed both metabolically and cognitively. Metabolic measures included fasting blood glucose, fasting insulin, and the HOMA-IR (Homeostasis Model Assessment of Insulin Resistance) index. Cognitive functions were evaluated using a standardized battery covering verbal and visual memory, attention, processing speed, executive function, and motor skills.  

Analyses revealed that higher fasting glucose and insulin levels, as well as a higher HOMA-IR, were significantly associated with poorer performance in several cognitive domains, particularly verbal memory, sustained attention, and processing speed. These associations persisted after adjusting for age, sex, BMI, illness duration, and antipsychotic treatment. The findings suggest a potential role of insulin resistance in cognitive decline, independent of other clinical factors.    


Caring for metabolism to protect the mind


Schizophrenia is a severe psychiatric disorder which, beyond its psychotic manifestations, is frequently accompanied by metabolic disturbances that can impair cognitive functions. The main challenge lies in jointly addressing psychiatric and metabolic dimensions to preserve patients’ overall functioning.  

The aim of this study was to explore the link between glucose homeostasis and cognitive performance, in order to identify new avenues for integrated care. The results highlight a significant association between impaired glucose regulation and cognitive deficits—especially in verbal memory and attention—suggesting that early metabolic monitoring could help preserve cognitive abilities and improve functional prognosis.  

Longitudinal studies will be needed to confirm these findings and support the systematic integration of metabolic follow-up in psychiatric care. They may also pave the way for the development of integrated therapeutic strategies combining antipsychotic treatment with targeted metabolic interventions, with the goal of optimizing both mental health and metabolic profiles in patients.

Read next: Can loneliness be read on the face?




About the author
 – Ana Espino
PhD in Immunology, specialized in Virology

As a scientific writer, Ana is passionate about bridging the gap between research and real-world impact. With expertise in immunology, virology, oncology, and clinical studies, she makes complex science clear and accessible. Her mission: to accelerate knowledge sharing and empower evidence-based decisions through impactful communication.




Source(s) :
Kancsev, A., et al. (2025). Glucose homeostasis and cognitive functions in schizophrenia: a systematic review and meta-analysis. Scientific reports, 15(1), 22898 ;

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