Increasing evidence suggests modulating effects of
cannabinoids on time of onset, severity, and outcome of
schizophrenia. Efforts to discover the underlying pathomechanism have led to the assumption of gene x environment interactions, including premorbid genetical vulnerability and worsening effects of continuing cannabis use. The objective of this cross-sectional study is to investigate the relationship between delta-9-tetrahydrocannabinol intake and
niacin sensitivity in
schizophrenia patients and healthy controls. Intensity of
niacin skin
flushing, indicating disturbed
prostaglandin-mediated processes, was used as peripheral marker of
lipid-
arachidonic acid pathways and investigated in cannabis-consuming and nonconsuming
schizophrenia patients and in healthy controls.
Methylnicotinate was applied in three concentrations onto the forearm skin. Flush response was assessed in 3-min intervals over 15 min using optical reflection spectroscopy. In controls, skin
flushing was significantly decreased in cannabis-consuming as compared to nonconsuming individuals. When comparing the nonconsuming subgroups, patients showed significantly decreased flush response. The populations as a whole (patients and controls) showed an inverse association between skin
flushing and sum scores of Symptom Check List 90-R. Results demonstrate an impact of long-term cannabis use on
lipid-
arachidonic acid pathways. Considering pre-existing vulnerability of lipid metabolism in
schizophrenia, observed effects of cannabis use support the notion of a gene x environment interaction.