We read with great interest the study of Barton et al,1 which provides new insights into brain serotonin metabolism and its possible implications in the pathogenesis of major depression by applying innovative, state-of-the-art techniques. We would like to raise 2 methodological issues.
To avoid a confounding effect of serotonergic neuronal systems activated by sunlight, Barton et al selected healthy volunteers from a large pool of subjects to achieve matching for sunlight hours on the day of the catheter sampling. However, even though sunlight duration may be a suitable measure of sunlight exposure in large epidemiological studies with homogenous samples, it may not be optimal when studying smaller and heterogeneous groups, such as patients with major depressive disorder (MDD) and healthy controls. In the latter case, individual history of exposure to sunlight could have been used in addition to sunlight duration. Depressed individuals may be less exposed to sunlight because of limited outdoor activities and thus the reported higher brain serotonin turnover in MDD cases compared with healthy individuals may actually be even more pronounced. Moreover, Barton et al took into consideration the sunlight duration corresponding only to the day of the blood sampling, probably based on their previous reported results that the brain serotonin turnover correlates significantly with the prevailing amount of bright sunlight on the day of the blood sampling but not to sunlight duration on the day before.2 In that study, the correlation of serotonin turnover with the mean sunlight duration during several days before the sampling day was not examined. On the other hand, it has been reported that light sensitivity in humans, as assessed by the magnitude of the suppression of melatonin secretion by nocturnal light, is affected by light exposure history during a week before the suppression test.3
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