Carbon monoxide: a critical physiological regulator sensitive to light

The mechanism by which humans absorb therapeutic light in winter seasonal and nonseasonal depression is unknown. Bright-light-induced release and generation of blood-borne gasotransmitters such as carbon monoxide (CO) may be one mechanism. Here, 24 healthy female volunteers had peripheral blood samples drawn. Samples were collected in a dimly lit room and protected from light exposure. Samples were analyzed for CO concentrations by gas chromatography after 2 h of continuous exposure to darkness vs. bright white light. In a similar confirmatory study, 11 additional volunteers had samples analyzed for CO concentrations after 2 h of continuous exposure to gentle rocking in darkness vs. in bright white light. In the first study, light-unexposed peripheral blood had a mean CO concentration of 1.8 ± 0.4 SD ppm/g. Identically treated samples with 2 h of rocking and exposure to bright white light at illuminance 10,000 lux had a mean CO of 3.6 ± 1.2 ppm/g (p < 0.0001). Post hoc analysis of that study showed that time of day was significantly inversely associated with increase in CO concentration under bright light vs. dark (p < 0.04). In a smaller confirmatory study of 11 healthy female volunteers, after 2 h of rocking, light-unexposed peripheral blood had a mean CO of 1.4 ± 0.5 SD ppm/g. Identically treated blood samples with 2 h of exposure to bright white light at illuminance 10,000 lux had a mean CO of 2.8 ± 1.7 ppm/g (p < 0.02). In conclusion, bright-light exposure robustly increases human blood CO in vitro. This supports the putative role of CO as a physiological regulator of circadian rhythms and light’s antidepressant effects. This human evidence replicates earlier data from a preclinical in vivo model. This effect may be stronger in the morning than in the afternoon.