The current study is a cross-sectional descriptive comparative study conducted in the institute of psychiatry Ain Shams University and Abbassia Mental Health Hospital from which a convenient sample of 60 subjects (40 cases and 20 control healthy subjects) fulfilling the inclusion criteria were recruited.
The present study aimed to evaluate the cognitive functions in a sample of patients with schizophrenia and test how metabolic syndrome can be a possible predictive risk for patients’ cognitive impairment.
Our results showed a significant difference between cases and controls’ cognitive functions and metabolic profile data. The case group had lower cognitive functions (TMT-A, TMT-B, WMS-R score) than controls. Similarly, patients with schizophrenia had a higher prevalence of high body mass index and high blood glucose levels compared to the control group. Despite the narrow differences between the groups’ BMI, however, the average percentage of obesity (BMI is ≥ 30) in schizophrenic patients was more than in the controls (BMI was between 25 and 30).
According to the previous researches, as many as 80% of patients with schizophrenia had cognitive dysfunctions, possibly as a core feature of the disease [16].
These results showed that all cases in the patients group had cognitive impairments. Those impairments were significantly higher than the controls, namely in the speed of processing and executive function, attention, and working memory scores TMT-A (p = 0.0), TMT-B (p = 0.00), and WMS-R (p = 0.029). On the other hand, there was no significant difference between the groups in the visual memory scores as shown in Table 1. This matched the study in a UK Biobank data which investigated the cognitive functions footprint of different psychiatric and neurological disorders in 2017 [17]. It revealed that 1.89–3.92% of the examined sample (n = 502,642) who were diagnosed as schizophrenic suffered from cognitive dysfunction in reasoning, pair matching, numeric memory, and reaction time [17].
Interestingly, the current data did not show a significant difference between case and control BMI. However, there was a significant difference between cases and control FBG levels (p = 0.00) as shown in Table 3, which matched Pillinger et al.’s [18] results, emphasizing on the fact that glucose homeostasis is altered in schizophrenic patients, indicating a high risk for diabetes in this population. Similarly, Kato and colleagues [19] reported that the body mass index does not differ significantly between schizophrenic and non-schizophrenic patients. On the contrary, Subramanian and colleagues [20] demonstrated that patients with schizophrenia were more prone to higher body weights than the healthy controls, attributing this difference to longer duration of illness, types of medication use, and presence of a comorbid medical condition.
This study found that the increase in patients’ BMI and FBG and not cholesterol level was associated with a decrease in candidates’ cognitive functions. This came in agreement with Guo and colleagues’ study [21] where they reported a significant correlation between the schizophrenic patients high BMI and low TMT-A, TMT-B, WMS-R Visual Reproduction subscale, and the WAIS Digit Symbol subscale scores (p ≤ 0.004) and was further confirmed by Hidese et al.’s study [22].
On the contrary, to some of our findings, some studies reported that hypertension followed by dyslipidemia were the most common vascular risks in schizophrenic patients and that increased body weight and elevated blood glucose were the least detected abnormality [19].
These study results found that high FBG followed by high BMI was the most involved factors in patients’ cognitive decline (TMT-A), while age of the patient, age of onset of disease, and duration of illness were the least significant factors.
In agreement with our results, Wysokiński and colleagues [23] concluded that dyslipidemia, raised LDL, and raised blood glucose levels were the best predictors of a more severe clinical and lower cognitive abilities (worse cognitive flexibility, executive functions, complex attention composite memory, verbal memory; slower reaction time; and worse performance) in schizophrenic patients. Also, Mosiołek’s [24] results which suggested that schizophrenic patients’ poor performance on the cognitive tasks compared to the healthy individuals occurs early in the course of the disease, yet stabilize across the age group.
Limitations and strength
This study is one of the rare studies testing the negative effects of the prevalent metabolic disorders in the schizophrenic population on their cognitive abilities. We used objective measures in testing patients’ cognitive abilities. Yet, the use of more scales in measuring patients’ cognitive abilities and other metabolic profile detectors such as waist circumference would have been more elaborative. In this study, we did not measure the levels of glycosylated hemoglobin, for logistic reasons, leaving us with nonconclusive data of the long-term effect of schizophrenia on glucose blood level control. Also, we did not measure the levels of cholesterol, triglyceride, and lipoprotein in healthy controls for limited financial resources. Moreover, we could not specify from history the main cause of diabetes or high fasting glucose level, leaving antipsychotic treatments, unhealthy lifestyle, and other factors as possible causes. Further longitudinal or a cross-sectional study with a larger number of cases from different hospitals in addition to bypassing the methodological limitations would have helped in the result generalization.