Letters to the EditorSerotonin and SIDSWarren G. GuntherothWarren G. GuntherothDepartment of Pediatrics (Cardiology), University of Washington, Seattle, WashingtonPublished Online:01 Oct 2011https://doi.org/10.1152/japplphysiol.00901.2011MoreSectionsPDF (27 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat to the editor: The article by Cummings et al. (2) emphasizes the vital role of serotonin in cardiovascular homeostasis and respiratory control, using mice with a genetic deficiency, challenged by severe and repeated anoxia. [Their model of an heritable defect as the cause of sudden infant death syndrome (SIDS) is not consistent with SIDS with a familial recurrence of only 16/1000 (4) and the incidence of all deaths after a SIDS case was 21/1000, indicating the lack of specificity of the recurrence.]Although the authors demonstrate that depletion of serotonin would increase the risk of death in these mice and that it may apply to SIDS, they do not discuss the possibility that an infant's failed efforts to survive would consume this essential substance. In short, are the serotonin abnormalities in the brain stem of SIDS victims the cause or the effect?Cann-Moison et al. (1) found that the levels of metabolites of serotonin and other neurotransmitters were elevated in cerebrospinal fluid of SIDS victims, as well as in infants who had survived severe asphyxia.Kinney, a coauthor of this paper, has postulated since 1994 that SIDS can be explained by a triple-risk hypothesis (3). These authors conclude that SIDS victims develop an abnormality of serotonergic cells during fetal life and are then born with a vulnerability that does not kill until 2–6 mo of age by a “stressor.” But Waggener (5) and three other groups prospectively tested a group of neonates who subsequently died of SIDS and found their respiratory function was no different from their controls.Finally, since the triple-risk hypothesis posits a defect originating in fetal life, by definition it is a congenital defect. The peak age of death for congenital defects is the first month of life; at that age the rate of SIDS is the lowest of the first year.The authors have performed their experiment well, but their extrapolation of the results to SIDS is unwarranted.REFERENCES1. Cann-Moisan C , Grinn E , Giroux JD , Le Bras P , Caroff J. Changes in cerebrospinal fluid monomine metabolites, tryptophan, and gamma-aminobutyric acid during the 1st year of life in normal infants: comparison with victims of sudden infant death syndrome. Biol Neonate 75: 153–159, 1999.Crossref | Google Scholar2. Cummings KJ , Commons KG , Hewitt JC , Daubenspeck JA , Li A , Kinney HC , Nattle EE. Failed heart rate recovery at a critical age in 5-HT-deficient mice exposed to episodic anoxia: Implications for SIDS. J Appl Physiol 111: 825–833, 2011.Link | ISI | Google Scholar3. Filiano JJ , Kinney HC. A perspective on neuropathologic findings in victims of the sudden infant death syndrome: the triple-risk model. Biol Neonate 65: 194–197, 1994.Crossref | PubMed | Google Scholar4. Guntheroth WG , Lohman R , Spiers PS. Risk of sudden infant death syndrome in subsequent siblings. J Pediatr 116: 520–524, 1990.Crossref | ISI | Google Scholar5. Waggener TB , Southall DP , Scott LA. Analysis of breathing patterns in a prospective population of term infants does not predict susceptibility to SIDS. Pediatr Res 27: 113–117, 1990.Crossref | ISI | Google ScholarAUTHOR NOTESAddress for reprint requests and other correspondence: W. G. Guntheroth, Dept. of Pediatrics (Cardiology), Univ. of Washington, Mail Stop 356320, Seattle, WA 98195 (e-mail: [email protected]edu). Download PDF Previous Back to Top Next FiguresReferencesRelatedInformationRelated articlesReply to Guntheroth 01 Oct 2011Journal of Applied Physiology More from this issue > Volume 111Issue 4October 2011Pages 1227-1227 Copyright & PermissionsCopyright © 2011 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00901.2011PubMed22566691History Published online 1 October 2011 Published in print 1 October 2011 Metrics