In this paper a detailed argument will be advanced in support of the notion that schizophrenia is fundamentally a diabetic brain state, henceforth referred to as 'cerebral diabetes'. Many extraneous features of cerebral diabetes have been observed, including positron emission tomography (PET) scans which reflect abnormal distribution patterns and diminished supplies of glucose in the brain. Equally, empirical research has demonstrated that plasma levels of essential fatty acids and prostaglandins are abnormally low, and low levels of glycoproteins in the urine of cerebral diabetics have also been observed. In addition, cerebral diabetics manifest a wide range of disturbing physical symptoms, such as, impaired sexual function, temperature control, low blood pressure, disrupted sleep patterns, excessive thirst, poor memory, insensitivity to pain, and chronic unhappiness, all of which can be attributed to disrupted neuroendocrine function. Thus, in order to persuasively assert the redefinition of schizophrenia as 'cerebral diabetes', we shall first explicate glucose regulation and transport in the brain and then outline how this interacts with essential fatty acids and prostaglandins, neurotransmission, and the neuroendocrine system. In so doing, we shall provide a metabolic explanation for all the prominent symptoms currently known to be associated with cerebral diabetes and indicate some future therapeutic interventions.