From Uppsala University
New insight into sudden infant death syndrome Sudden infant death syndrome (SIDS) usually affects infants during their first six months of life. The incidence of this disease in Sweden increased during the 1980’s and was approximately one death in 1000 live births in 1990 and was considerably greater in some other countries. After 1992-1993 the incidence of this disease has decreased to a level of approximately one third of that in 1990. This decrease has been considered not only to be associated with the recommendation to parents not to place the babies in the prone position during sleep but also with an intense propaganda to breast feed the infants, and to abstain from smoking during pregnancy and the infant’s first six months of life. In addition to this a too warm sleep environment and excess bedclothing are known risk factors. However, the true mechanisms behind SIDS remain unknown.
In 1997 professor Lars Wiklund and his co-workers published results that demonstrated that victims of SIDS, in contrast to those who died from other causes, had an enteric microflora that was not capable of metabolising urea to ammonium ion, urea being a natural component of both human breast milk and cow’s milk. The hypothesis was that this resulted in alkalinisation of the baby that was forced to compensate by lowering of the carbon dioxide elimination by reducing the pulmonary ventilation. This could lead to unconsciousness and worsen breathing. Unless this sequence of events was stopped it could result in death. The hypothesis is in agreement with previously recognised risk factors. The prone position e.g. results in a higher body temperature which leads to a higher carbon dioxide tension and subsequently sometimes to unconsciousness and an increased risk of death. In the same study it was also shown that the urea metabolising enteric bacteria produce nitric oxide in small amounts, the concentration of which was correlated to the remaining unmetabolised urea content in faeces. It was also shown that very small amounts of nitrate and nitrite inhibit the urea metabolism of the enteric microflora.
As nitrate in these small concentrations could inhibit the urea metabolism of urea it could be presumed that the nitrate content in drinking water could contribute to the occurrence of SIDS especially as the concentration of nitrate in groundwater and drinking water is known to vary, being greatest during early spring, and least during summer and during winter when the soil is frozen. It is well known that the incidence of the disease has a similar pattern. In order to elucidate the possible effects of nitrate in the drinking water Mary George and her co-workers at Uppsala University examined slightly more than 600 SIDS cases that occurred during the period 1990 to 1996 in Sweden. The results showed that the deaths in the far north occurred during the time when practically no SIDS deaths at all occurred in the south of the country. The results also showed that there was an association between the time when the deaths occurred and increasing or maximal groundwater levels as well as between the local incidence of deaths and the maximally recorded nitrate concentration in drinking water.
The conclusion so far would be that the hypothesis of an inhibited enteric bacterial metabolism of urea as one cause of SIDS still seems to be interesting and possibly valid.
The investigation, that was conducted by the pediatric anaesthesist Mary George in co-operation with the professor of cancer epidemiology Lars Holmberg, the water geologists Mats Aastrup, Jan Pousette and Bo Thunholm, the professor of forensic medicine Tom Saldeen and the professor of anaesthesiology Lars Wiklund has just been published in the December issue of the European Journal of Clinical Investigation.