Sudden Infant Death Syndrome (SIDS), also known as Crib Death Syndrome, is one of the most dramatic and to date unexplained events leading to the death of newborns (peaking between 2 and 4 months of age), apparently healthy and the one in Italy, the Ministry of Health, estimates could cover 250 new cases per year.
A new study from the United States shows that the cause of SIDS of could be biological nature. Researchers at Boston Children’s Hospital, led by Robin L. Haynes, analyzed the brain stems of 70 babies who died between 2004 and 2011 and who had brain abnormalities. They found that the serotonin 2A/C receptor (serotonin is a neurotransmitter) affected the deaths of SIDs.
Previous research in rodents had shown that the receptor in question plays a role in “awakening” and the ability to “self-resuscitate” by playing a role in protecting cerebral oxygenation during sleep. The new research therefore supports the idea that a biological abnormality may make some infants more vulnerable to SIDS, and that the syndrome may be promoted by three co-occurring conditions: the infant is in a critical stage of cardiorespiratory development (in the first year of life), the child experiences a stressful situation caused by the position it adopts during sleep (when lying on its stomach or sharing the bed with someone), the child has a biological abnormality that puts it at risk of breathing difficulties during sleep.
“While we have identified serotonin 2A/C receptor abnormalities associated with SIDS, the relationship between these abnormalities and cause of death remains unknown. The consequences of the anomalies in this receptor in the context of a broader network of receptors that protect the vital functions of cardiac and respiratory control when the subject faces severe stress conditions remain to be explored. There is currently no way to preemptively identify neonates with biological abnormalities in the serotonergic system. Therefore, adherence to “safe sleep” practices remains the only valid weapon for SIDS prevention,” explains Haynes.
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