## 1 Introduction  
There is a general consensus that somatic comorbidity largely accounts for reduced life expectancy in people with schizophrenia [1]. It has been demonstrated that cardiovascular diseases are among the leading causes of mortality in this clinical population [2]. Studies show that about 30% of individuals with schizophrenia develop metabolic syndrome, which is a clustering of visceral obesity, atherogenic dyslipidemia, insulin resistance and hypertension [3]. To date, a variety of factors contributing to this phenomenon have been identified. These mainly include lifestyle factors (unhealthy dietary patterns, low physical activity and cigarette smoking) and the effects of psychopharmaceutical treatment [4]. However, there is robust evidence that subclinical metabolic abnormalities, such as lipid profile disturbances [5], impaired glucose homeostasis [6] and subclinical inflammation, occur at the onset of psychosis [7; 8]. This suggests that other mechanisms, intrinsic to the pathophysiology of psychosis, might impact cardiovascular risk among people with schizophrenia [9].  
Accumulating evidence indicates high heterogeneity of schizophrenia in terms of its clinical manifestation and outcomes. In 1988, [PERSON] et al. proposed to dissect the deficit schizophrenia subtype (D-SCZ), which manifests as primary and enduring negative symptoms [10]. Subsequently, it has been observed that patients with D-SCZ show unfavorable clinical and functional outcomes, which are likely attributable to greater cognitive deficits as well as neurostructural and neurofunctional alterations [11; 12; 13]. Some studies indicate that patients with D-SCZ might be at higher cardiovascular risk. For instance, [PERSON] et al. [14] found that patients with D-SCZ are at greater risk of fatal outcomes during coronary heart disease and that they are more likely to develop obesity than those with nondeficit schizophrenia (ND-SCZ). In turn, another study performed on a smaller sample observed no significant differences in cardiovascular indicators between individuals with D-SCZ and those with ND-SCZ [15]. There are also studies showing elevated concentrations of inflammatory cytokines and C-reactive protein (CRP) in patients with D-SCZ in comparison with patients diagnosed with ND-SCZ and healthy controls [16; 17].  
The mechanisms underlying the association of elevated cardiovascular risk and D-SCZ remain unknown. Notably, previous studies investigating these associations have not controlled for the effects of several lifestyle characteristics. It has been found that patients with schizophrenia have unhealthy dietary habits that might predispose them to develop obesity, type 2 diabetes and cardiovascular complications [18; 19]. Moreover, individuals with schizophrenia show less physical activity and more sedentary behavior [20]. Some studies also indicate that unhealthy dietary habits and low levels of physical activity might be associated with higher levels of negative symptoms [21; 22]. Following these considerations, we aimed to compare the lipid profile, glucose homeostasis parameters and CRP levels between patients with D-SCZ, patients with ND-SCZ and healthy controls after adjustment for the effects of lifestyle characteristics. Furthermore, we tested the hypothesis that cardiovascular alterations are related to psychopathological manifestations and cognitive performance in patients with schizophrenia.