On 2015 Jan 25, David Mage commented:

We (Mage and Donner) agree 100% with the authors' conclusion that there could be a commonality of the terminal mechanisms of SIDS and SUDEP. Our research on SIDS, based upon the universal 50% SIDS male excess for equal numbers of males and females at risk, predicts that the SIDS causation is X-linked resulting in acute anoxic encephalopathy (See our abstracts 9076695, 15384886 and 24164639). We suggested that a presently unknown gene locus on the X with a protective dominant allele with frequency p = 1/3 is involved. It would code for a protein enzyme that would allow the respiratory control neurons in the brainstem to shift from aerobic oxidation to anaerobic oxidation during a transient episode of acute cerebral anoxia. The XY male would be at risk of not having this dominant ability with frequency q = 2/3 and the XX female would be at identical risk with frequency q x q = 4/9. For equal numbers of male and female infants at risk the ratio 2/3 to 4/9 = 1.5, giving the expectation of 3 males dying of SIDS for every 2 females dying of SIDS. The authors report that for their cited 85 cases of prone SUDEP that there were 51 male and 34 female patients which is exactly in the ratio of 3 male to 2 female as we predicted. They propose that the main mechanism of SUDEP in their study is the peripheral hypoventilation and suffocation secondary to complete or partial airway obstruction which could lead to potentially terminal acute cerebral anoxia. We suggest that this may be a fertile field for further investigation because, to our knowledge, there is no other hypothesis in the medical literature that can predict that both SIDS and SUDEP would have the same 50% male excess.

On 2015 Jan 25, David Mage commented:

We (Mage and Donner) agree 100% with the authors' conclusion that there could be a commonality of the terminal mechanisms of SIDS and SUDEP. Our research on SIDS, based upon the universal 50% SIDS male excess for equal numbers of males and females at risk, predicts that the SIDS causation is X-linked resulting in acute anoxic encephalopathy (See our abstracts 9076695, 15384886 and 24164639). We suggested that a presently unknown gene locus on the X with a protective dominant allele with frequency p = 1/3 is involved. It would code for a protein enzyme that would allow the respiratory control neurons in the brainstem to shift from aerobic oxidation to anaerobic oxidation during a transient episode of acute cerebral anoxia. The XY male would be at risk of not having this dominant ability with frequency q = 2/3 and the XX female would be at identical risk with frequency q x q = 4/9. For equal numbers of male and female infants at risk the ratio 2/3 to 4/9 = 1.5, giving the expectation of 3 males dying of SIDS for every 2 females dying of SIDS. The authors report that for their cited 85 cases of prone SUDEP that there were 51 male and 34 female patients which is exactly in the ratio of 3 male to 2 female as we predicted. They propose that the main mechanism of SUDEP in their study is the peripheral hypoventilation and suffocation secondary to complete or partial airway obstruction which could lead to potentially terminal acute cerebral anoxia. We suggest that this may be a fertile field for further investigation because, to our knowledge, there is no other hypothesis in the medical literature that can predict that both SIDS and SUDEP would have the same 50% male excess.