Sudden infant death syndrome (SIDS) is one of the leading causes of infant mortality in the US. It causes around 2,400 deaths every year, and the majority of previous studies have concluded that there is no specific cause. But, could genetics play a part in the risks of SIDS? A new study has suggested that it could.

In the study, researchers found that newborn babies who were born with a specific genetic mutation, SCN4A, which plays a role in regulating muscle control , could have an increased risk. The SCN4A gene is very rare, affecting less than five people per 100,000, however it can cause a range of conditions including spasms which lead to breathing and speech difficulties. It’s thought that the weakening of the muscles used for breathing could be to blame in some cases of SIDS.

This isn’t the first time breathing problems have been blamed for cot death. Although the cause is still unknown, advice is often give to parents like avoiding co-sleeping or making sure babies are put to sleep on their back. This measures have been proven to reduce the risks, so there’s a possibility this is also linked to babies breathing.

Professor Michael Hanna, from the Medical Research Council Centre for Neuromuscular Diseases at University College London, said: “Our study is the first to link a genetic cause of weaker breathing muscles with sudden infant death syndrome, and suggests that genes controlling breathing muscle function could be important in this condition.”

“However, more research will be needed to confirm and fully understand this link. While there are drug treatments for children and adults with genetic neuromuscular disorders caused by SCN4A gene mutations, it is unclear whether these treatments would reduce the risk of sudden infant death syndrome, and further research is essential before these findings can become relevant to treatment.”

Dr Stephen Cannon, from the University of California in Los Angeles, added: “A better understanding of the causes of Sids is needed to identify infants at high risk and to develop interventions and guidelines that will prevent Sids for all infants. Overall, the evidence is compelling that variants of SCN4A with disruption of channel function are over-represented in Sids.”

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