Published online 2 February 2010 | Nature | doi:10.1038/news.2010.49


Cot death victims make less serotonin

Mysterious infant deaths linked to chemical deficiency.

BabyResearchers have linked serotonin deficiency to SIDS.iStockPhoto

Babies killed by sudden infant death syndrome (SIDS) — also known as cot death — often have unusually low levels of a critical chemical called serotonin in their brains, researchers have found.

Serotonin acts in the brain stem to regulate heart rate, breathing and arousal from sleep. Lower levels of serotonin could explain why some babies may fail to properly respond to suffocation or overheating during the night, according to a study published this week in the Journal of the American Medical Association1.

SIDS is the third most common cause of death in infants in the United States, claiming the lives of roughly 1 out of every 2,000 babies in the country. The figure varies widely around the world, with Japan having 0.09 cases per 1000 infants — the lowest rate in the world — and New Zealand with 0.8 per 1000 — the highest. But despite decades of research, scientists still do not fully understand why some seemingly healthy babies die in their sleep.

What is clear is that the incidence of SIDS dropped dramatically after a large public health campaign encouraged parents to put babies to sleep on their backs — rather than on their stomachs or their sides — and to keep cribs free from soft bedding that might smother infants. This success demonstrated that environmental risk factors contribute to the syndrome but do not fully account for the deaths.

"We still have babies dying on their backs," says Marian Willinger, who directs the SIDS research program at the US National Institute of Child Health and Human Development in Bethesda, Maryland, which funded the new study. "And that's why the basic research has to continue."

Hunting a killer

In 2006, pathologist Hannah Kinney of Children's Hospital Boston and her colleagues reported that babies who die of SIDS often do not have as many serotonin receptors as babies who died of other causes in regions of the brain stem that coordinate responses to changes in oxygen and carbon dioxide concentration2. At that time, however, it was not clear if the concentration of serotonin itself was affected.

Since then, Kinney and her team have compared serotonin levels in the brain stems of 35 children who died of SIDS to those in the brain stems of 10 children who died of other causes, including 5 who experienced a lack of oxygen, as did the babies who died of SIDS. Their results now show that serotonin levels are 26% lower in the SIDS victims and levels of a key enzyme in serotonin synthesis, called tryptophan hydroxylase, was reduced by 22%.


"It's an important next step," says Rachel Moon, a paediatrician at Children's National Medical Center in Washington DC, who was not involved with the work. "It gives more credence to the argument that these babies are physiologically different from other babies, and that difference puts them at higher risk."

At this stage it is unclear whether reduced serotonin levels are a cause or an effect of SIDS, but Kinney hopes that this new clue will help her team trace the underlying molecular changes that make some children more vulnerable. Eventually, such work could lead to a test to identify such babies or an intervention to protect them.

In the meantime, Kinney, who decided she would study SIDS after trying and failing to resuscitate a SIDS baby as a paediatric resident, refers to her results when she consoles grieving parents. "What this means to them is that SIDS is an intrinsic biologic process," she says. "It's not something the parents did. You couldn't predict what night this was going to happen to their child." 

  • References

    1. Duncan, J. R. et al. JAMA 303, 430-437 (2010). | Article
    2. Paterson, D. S. et al. JAMA 296, 2124-2132 (2006). | Article | PubMed | ChemPort |
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