Research Highlights: Serotonin and Tryptophan Hydroxylase Deficiency Found in SIDS Infants

Serotonin and Tryptophan Hydroxylase Deficiency Found in SIDS Infants
Caroline Melhado

The Journal of the American Medical Association recently published a Harvard based finding that states babies who die of Sudden Infant Death Syndrome (SIDS) are most likely to have a decreased level of serotonin and its biosynthetic enzyme TPH2, tryptophan hydroxylase, when compared to control children. These lower levels would normally lead to a diagnosis of medullary 5-HT (serotonin) deficiency disorder, if caught before death.

Previous hypothesis of SIDS speculated that death was due to the inability of a baby to self-arouse after a life threatening event, such as asphyxia. The study aimed to find whether the inability to return to homeostasis was due to an elevated or decreased serotonin production. The study included post-mortem evaluations of serotonin and tissue from 41 infants. 7 infants, wh had died from known causes other than SIDS were used as controls, as well as 5 infants who were hospitalized with chronic hypoxia-ischemia.

Researchers found that serotonin levels were 26% lower in babies who had died of SIDS. Tissue collection from the raphé obscurus showed levels of TPH2 were 22% lower in SIDS cases than in controls. The ratio between serotonin and TPH2 was consistent throughout both the SIDS cases and control cases.

From these results researchers extrapolated that SIDS death most likely due to the insufficient amount of serotonin, due to the decreased levels of TPH2, to self-arouse during asphyxia. Authors of the study hypothesize that the low levels of TPH2 result from some unknown developmental reason, probably in the first or second trimester, that leads to the production of immature serotonin receptor binding sites and decreased levels of serotonin. Further animal testing might divulge how decreased levels of TPH2 arise during embryonic development and how this deficiency leads to sudden death during sleep.

JAMA. 2010;303(5):430-437.