Seasonal fluctuation in schizophrenia.

Abstract

Back to table of contents Previous article Next article Letter to the EditorFull AccessSeasonal Fluctuation in SchizophreniaMARKUS FRITZSCHE, M.D., , and JÜRG SCHMIDLI, PH.D., MARKUS FRITZSCHESearch for more papers by this author, M.D., Adliswil, Switzerland, and JÜRG SCHMIDLISearch for more papers by this author, PH.D., Zurich, SwitzerlandPublished Online:1 Mar 2002https://doi.org/10.1176/appi.ajp.159.3.499-aAboutSectionsView EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: Jaana M. Suvisaari, M.D., Ph.D., and her colleagues suggested in their intriguing article (1) that procreation in the summertime represents a constant hazard, in addition to an irregular environmental risk factor, for schizophrenia. Are these two components independent variables or just two facets of a common pathogenic mechanism that might ultimately be preventable?Using a novel climatic data set (2, 3), we compared their data with mean temperature and precipitation rates over the same time. The dramatic multiyear fluctuations, particularly the odds amplitude for patients born in 1955–1959, cannot be explained by the subtle climatic variations, neither in the more densely populated southern part nor in the rest of Finland. The fluctuations in schizophrenia births, which have also been reported from Denmark and Scotland (4), might rather be related to an additional stochastic factor prevalent in the north.In comparison to the first account by Tramer (5), the reported data, showing the lower schizophrenic birth rates in July through August (1955–1959), reveal another potential clue to the environmental determinant of schizophrenia. In Switzerland, we have, in addition to the widely replicated excess of schizophrenia births in the winter and spring months, a second minor peak in July (5). This bimodal distribution mirrors the seasonal concentration of ticks (Ixodes ricinus) 9 months earlier, with a major peak in spring and a minor peak in autumn separated by a decrease in humidity in the summer (6). Ticks containing Borrelia burgdorferi are prevalent in the urban recreational areas of Helsinki. However, as in the Alps, the minimal mean temperature of 7°C required for tick activity (6) allows only one peak from May to September in Finland, during which time the annual precipitation is also highest. Tick activity coinciding with procreational preference in the summertime might thus represent the stable component. While a few autumn-feeding I. ricinus ticks are still active up to November in central Europe (6), the temperature falls below 0°C in Finland. Adverse weather conditions, known to underlie the stochastic year-to-year oscillations of tick populations (7, 8), might thus reflect the irregular component of schizophrenia births in the north.Contrary to the current belief shared by Dr. Suvisaari et al. and others, neither the excess of schizophrenia winter births nor the excess of schizophrenia itself occurs at a constant rate worldwide. South of the Wallace line (9, 10), which limits the southward spread of species, including B. burgdorferi-transmitting ticks (6), seasonal schizophrenia trends appear to be insignificant or nonexistent, and in certain remote areas schizophrenia is even absent (11). We found only one psychotic patient in a neuropsychiatric survey comprising over 10,000 Papuans in the interior of New Guinea—fewer than expected (12). In Australia, where Borrelia garini is only sporadically introduced by migratory seabirds, B. burgdorferi could not be detected and cannot be transmitted by the local tick, I. holocyclus. It is not surprising after all that the higher rates of schizophrenia have been reported from the northeastern, northwestern, and Great Lakes states, which score the highest numbers of Ixoid tick populations and infections by B. burgdorferi(13).An early prenatal event interfering with neuronal migration has been suggested to underlie the consistent pattern of cellular disarray observed in schizophrenia brains. This hypothesis, however, contrasts with the reported pregnancy and birth complications during the second and third trimesters related to hypoxic damage or viral infections, as suggested by Dr. Suvisaari et al. and others. However, since B. burgdorferi has direct access to host genes, which the intracellular pathogen exploits like a virus for its own replication, a novel mutation might thus affect a gene prone to be hit by B. burgdorferi, the cannabinoid receptor gene (14), which is known to induce both hypoxic resistance and neuronal migration.