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Evidence is mounting that decreased levels of serotonin in brain tissues is associated with sudden infant death syndrome (SIDS).
Evidence is mounting that decreased levels of serotonin in brain tissues is associated with sudden infant death syndrome (SIDS). Researchers believe that a lack of serotonin, which is thought to be crucial to a baby’s arousal system, hampers a sleeping baby’s ability to wake up when his or her safety is threatened by a lack of oxygen or some other hazard. The serotonin deficit in some babies may be caused by a birth defect.
Hannah C Kinney, MD, has led some of the most recent research on this hypothesis. In a study published in the Journal of the American Medical Association, she and her colleagues demonstrated that SIDS is associated with reductions in brain tissue levels of serotonin (5-HT); its key biosynthetic enzyme, TPH2; or both. The researchers collected tissue samples from infants who died from SIDS and those who died acutely in whom a definitive cause of death was established (controls). Serotonin levels were 26% lower in the infants with SIDS, compared with age-adjusted controls. TPH2 levels were also were lower-by 22%-in the SIDS infants.
Investigators found no associations between SIDS risk factors such as sleep position or prematurity and 5-HT. Nonetheless, at least 1 risk factor was present in 95% of the SIDS cases and 2 or more risk factors in 88%. Noting that this finding further underscores that SIDS results from the simultaneous occurrence of multiple events, these researchers and other serotonin researchers believe that physicians should continue providing parents with “back to sleep” and other accepted safe sleep recommendations for limiting SIDS deaths.
Duncan JR, Paterson DS, Hoffman JM, et al. Brainstem serotonergic deficiency in sudden infant death syndrome. JAMA. 2010;303(5):430-437.