Researchers are feverishly pursuing pharmacological treatments for cognitive dysfunction in schizophrenia (2). Several mechanisms are being targeted, such as α7 nicotinic receptor agonists, dopamine D1 receptor agonists, AMPA glutamatergic receptor agonists, α2-adrenergic agonists, N-methyl-d-aspartate glutamatergic receptors, γ-aminobutyric acid receptor agonists, and others (9). Most researchers assume that cognitive deficits are part of the genetic etiology of schizophrenia, as evidenced by their presence in first-degree relatives (10). However, nongenetic (secondary) factors in cognitive impairments have been attributed to lifestyle factors (isolation and lack of stimulation), antipsychotic treatment factors (excessive dopamine receptor blockade), and the use of anticholinergic medications to mitigate iatrogenic movement disorders, such as parkinsonism and dyskinesia (11). Similarly, metabolic disorders in schizophrenia have been attributed to genetic factors, which could explain the higher visceral adiposity and glucose dysregulation at the onset of psychosis in drug-naive schizophrenia patients, which may later worsen due to lifestyle factors (sedentary living, high caloric intake) and antipsychotic drug side effects (increased appetite and loss of satiety). The bottom line, however, is that regardless of etiology, interventions to reduce obesity and hypertension (diet, exercise, and cognitive remediation and/or antihypertensive medication) may have a salutary effect on both cognitive deficits and metabolic disorders and may reduce the dual grave outcomes of functional disability and cardiovascular risk.