The diagnostic concept of “schizophrenia” is over 100 years old. It was developed at a time when medical laboratory testing barely existed. The concept of schizophrenia was based on behavioral observations interpreted in the light of the dominant theories of the day. Those theories were based on the concepts of Freudian psychodynamics, germ theories of infection, and nerve degeneration. Those theories of causation have been almost entirely discredited as causes of schizophrenia.
The modern definition of schizophrenia has retained many of the original ideas, diverse as they are. The modern definition of schizophrenia undoubtedly captures a population of individuals who are similar only on a superficial level. Though outward behavioral symptoms may look similar, the underlying disease processes are numerous and distinctly different. This underlying diversity of biological cause is the best explanation for why some with schizophrenia derive rapid robust benefit from medication while others with similar outward symptoms are not helped by the same medication.
My major current research interest is the unusually sluggish response to niacin often seen in schizophrenia. Pharmacological doses of niacin cause most people to have a skin flush response. A similar skin flush response occurs when a sufficiently high concentration of methyl-niacin is applied to the skin. Many people with schizophrenia do not have a skin flush response to niacin.
The blunted skin flush response to niacin is interesting for several reasons:
Potential applications of the niacin skin test