PLOS Med | Data from nearly 1.3 million people suggest that insulin resistance and schizophrenia have a common mechanism of action!

Schizophrenia is a complex behavioral and cognitive syndrome, the main characteristic of which is disturbance of perception and cognition.

The lifetime prevalence of spermatozoa is about 0.

Usually, the myocardial metabolism disorder of schizophrenia patients is attributed to the adverse effects of antipsychotic drugs or poor lifestyle factors, such as lack of exercise and eating habits, but the above-mentioned mechanisms cannot fully explain this phenomenon.

Elevated fasting insulin, elevated triglycerides, and low high-density lipoprotein (HDL) cholesterol , that is, insulin resistance, are associated with first-onset psychosis (FEP) in relatively young antipsychotic asymptomatic patients.

Diabetes may be causally related to schizophrenia, or have a common pathophysiological mechanism with schizophrenia.

At present, there is little evidence that inflammation may be a common mechanism of schizophrenia and cardiometabolic diseases.

Inflammation may be a common mechanism of schizophrenia and cardiometabolic diseases.

The researchers used aggregated data from six large consortia association studies, namely the whole genome of the Consortium for Glucose and Insulin Related Traits (MAGIC), with 108,557 participants; Diabetes Genetic Replication and Meta-Analysis (DIAGRAM) with 435387 people.

Two samples of univariate and multivariate Mendelian randomization (MR) analysis were performed on the above participants to test: (i) 10 cardiometabolic traits (fasting insulin, high-density lipoprotein, and high-density lipoprotein, which represent the insulin resistance phenotype) Triglycerides, and 7 related cardiometabolic traits, low-density lipoprotein, fasting plasma glucose, glycosylated hemoglobin, leptin, body mass index, glucose tolerance and type 2 diabetes) may be causally related to schizophrenia; (ii) Whether inflammation may be the common mechanism of these phenotypes.

In general, the results of the study did not find statistically significant evidence to support a causal relationship between cardiometabolic characteristics and schizophrenia, or vice versa.

Gene-predicted inflammation-related insulin resistance phenotypes (such as increased fasting insulin (Wald ratio OR=2.

After adjusting for CRP, the evidence for these associations was reduced to zero in the multivariate MR analysis, indicating that the above-mentioned association between insulin resistance and schizophrenia can be completely explained by inflammation.

The link between insulin resistance and schizophrenia can be explained entirely by inflammation.

In summary, the results of this study support the role of inflammation as a common mechanism of insulin resistance and schizophrenia.

references:

Perry BI, et al.

plos.
org/plosmedicine/article?id=10.
1371/journal.
pmed.
1003455" target="_blank" rel="noopener">The potential shared role of inflammation in insulin resistance and schizophrenia: A bidirectional two-sample mendelian randomization study.


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