05/13/2022
In the last few days, I have seen many posts celebrating the new study just released by Carmel Harrington at the SIDS and Sleep Apnea Research Group, New South Wales, Australia, where they have identified a possible link in an enzyme deficiency and an increased risk of SIDS. This is all very exciting, but what does it actually mean and what happens next?
Sudden Infant Death Syndrome (SIDS) is the fear every new parent has. Scientists and doctors don't yet understand the actual cause of SIDS, but through years of research and collecting data have identified five risk factors for SIDS
- S*x. Boys are slightly more likely to die of SIDS.
- Age. Infants are most vulnerable between the second and fourth months of life.
- Race. For reasons that aren't well-understood, non-white infants are more likely to develop SIDS.
- Family history of SIDS
- Secondhand smoke.
- Low birth weight, prematurity
Researchers have also identified a Triple Risk Model, which helps us understand how the risk factors for SIDS interact. The Triple Risk Model poses that a vulnerable baby at a critical period in development, when exposed to an external stressor with which they are unable to cope, may die from SIDS.
The Back to Sleep campaign was launched in 1994, and through education on safe sleep practices, cases of SIDS were reduced by 50% by the year 2000.
Researchers have thought for some time that infant arousal levels may be a factor that makes them more vulnerable to SIDS, and this new study seems to support that thinking.
The new Harrington study is a small case-control study of 67 infants whose deaths were classified as a sudden unexpected death. Blood spots were taken from routine newborn blood screening at birth and compared with gender and date of birth matched surviving infants within the study.
An enzyme called butyrylcholinesterase (BChE) was found in lower levels in the blood of the infants who died.
BChE plays a role in the brain's arousal pathway. Researchers believe its deficiency likely indicates an arousal deficit, which could reduce an infant's ability to wake or respond to the external environment, causing vulnerability to SIDS.
Put more simply, if a baby were to roll onto their stomach and their breathing became compromised, they may be breathing in exhaled carbon dioxide. Eventually, their oxygen level would drop. Usually, once their brain recognizes the drop in oxygen, the baby would startle awake and cry out for help. Potentially a baby with lower levels of BChE may not have the same arousal response and therefore would be susceptible to SIDS.
While this is potentially an amazing breakthrough, it raises many questions and much more research is needed.
The next step for researchers is to begin looking at introducing the BChE biomarker into newborn screening and developing specific interventions to address the enzyme deficiency. It is expected this will take around five years to complete.
Could it possibly be as simple as identifying lower levels of BChE at birth and supplementing to 'normal' levels, and could that potentially bring a broader complacency about safe sleeping environments?
If there is no possibility of supplementing BChE, what are the implications of parents being told their babies are at higher risk for SIDS, and how do we then support these parents?
Either way, we must continue to practice and advocate safe sleep guidelines and practices at all times by ensuring babies are placed on their backs, on a flat and firm mattress, and have nothing else in their sleep space with them, ensuring that airways are not obstructed in any fashion, baby has open-air around them to breathe and encourage room sharing, specifically being within sensory range of a sober, dedicated adult caregiver.
https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(22)00222-5/fulltext----
BChEsa, measured in dried blood spots taken 2-3 days after birth, was lower in babies who subsequently died of SIDS compared to surviving controls and other Non-SIDS deaths. We conclude that a previously unidentified cholinergic deficit, identifiable by abnormal -BChEsa, is present at birth in SIDS....