SIDS-CDF hypothesis revisited: explaining hypoxia in SIDS

Sudden infant death syndrome and the diaphragm: Is there a link?

“…Pathogenic gene variants of SCN4A that encode for NaV1. 4, a skeletal muscle voltage-gated sodium channel that is crucial for the generation of action potentials and excitation of muscle, are overrepresented in infants who died of SIDS compared with ethnically matched controls. These functionally disruptive SCN4A variants can impair the ability of respiratory muscles to respond to hypoxia.…”

“…3 Hypoxia exacerbates diaphragm and abdominal muscle fatigability and can impair the diaphragm's ability to generate force. 4 3. There is a strong correlation between SIDS and nonlethal infections.…”

“…3 Hypoxia exacerbates diaphragm and abdominal muscle fatigability and can impair the diaphragm’s ability to generate force. 4 There is a strong correlation between SIDS and nonlethal infections. It is well known that infections can produce severe respiratory muscle weakness in adults, which is a major contributor to respiratory failure.…”

“…3 Hypoxia exacerbates diaphragm and abdominal muscle fatigability and can impair the diaphragm’s ability to generate force. 4 …”

SIDS–CDF Hypothesis Revisited: Cause vs. Contributing Factors

“…The basic premise of the hypothesis is that the diaphragm is a vital organ that must continuously generate adequate force to maintain ventilation, and that CDF is a terminal event and the cause of death in SIDS. I have argued in two follow-up articles that all SIDS factors either increase the workload of the respiratory muscles, the diaphragm being the primary muscle affected, or reduce its force generating capacity (6, 7). The SIDS–CDF hypothesis posits that SIDS has many contributing factors but only one cause, namely, the failure of the vital respiratory pump.…”