Another new theory explaining the cause of SIDS

Abstract

A great number of theories explaining the cause of the Sudden Infant Death Syndrome (SIDS) have been published during the last decades, many in so-called `high-impact' journals. In fact, few diseases in paediatrics have inspired so many scientists in various fields to solve the enigma why apparently healthy infants suddenly die. A new study was recently published in JAMA by Paterson et al. (1). The authors reported that victims of SIDS have a decreased binding of serotonin in some important brain nuclei involved in sleep and respiration. The reduced receptor binding density was particularly seen in the male SIDS cases. This finding confirms a previous observation by Ozawa et al. (2). Furthermore, Paterson et al. found a significantly higher serotonin neuron density in medullary nuclei involved in homeostatic function. These findings are very thought-provoking and also fit into the well-established finding that sleeping in prone position increases the risk. Infants who lie with the face down towards the mattress may develop desaturation and carbon dioxide retention. Normally, this should result in arousal and awakening of the infant, but deficiencies involving serotonin containing nuclei may hazard this mechanism. It is interesting that serotonin has been proposed to play a crucial role in the CO2-sensitivity (3). The finding of more marked disturbances of the serotonin system in the male SIDS cases also fit with the higher incidence of SIDS among boys. Furthermore, Weese-Mayer et al. have demonstrated that victims of SIDS often has a mutation of the PHOX2b gene, which is involved in the encoding of the serotonin synthesizing enzymes (4). This was mainly found in Afro-American infants who have a high risk of dying of SIDS. The findings are novel and of considerable interest to understand the mechanisms causing SIDS. However, the limitations of this study have also been pointed out in an Editorial in JAMA (5). The size of the study group is relatively small, with only 31 index infants and 10 control cases. The main problem is that one third of the index cases were ex-preterm infants. Although prematurity is a well-known risk factor for SIDS it cannot be excluded that the differences between the SIDS victims and the controls may be due to immaturity. Only one of the ten controls was born preterm. The finding that the expression of neurotransmitters and their receptors may be disturbed in SIDS victims is not new. The same research group has earlier reported changes of muscarinic receptors (6). Neuropeptides like substance P have also been found to be different in SIDS victims (7). Furthermore, nicotinic receptors may also be involved, since maternal smoking is one of the most important risk factors causing SIDS (8). The current findings were published in a high-impact journal and aroused a lot of media attention and were presented in the CNN news nearly every hour on the day they were published, like many other new hypotheses on SIDS (Fig. 1). This can be compared with the first reports suggesting the importance of putting the baby in a back position instead of a prone position (9-11). It took some time before they attracted attention, resulting in the most successful prevention of SIDS. Some theories on the cause of SIDS published in the New England Journal of Medicine.