The sudden infant death syndrome (SIDS) is a fatal dysautonomia of unknown cause that some studies have connected to energy metabolism. Unfortunately, SIDS appears to be common in these families before the diagnosis of mitochondrial disease is made. When the diagnosis is made, families are told to prevent fasting and to go to an emergency room for IV (high-dose) sugar-containing fluids if their child takes in a lot less calories or has vomiting (associated with a viral illness, vaccination, etc.). Several episodes in infants and toddlers of severe acidosis and/or hypoglycemia that likely would have proceeded to death have been prevented in this manner. Dr. Boles has previously reported that 20% of a large group of SIDS babies had essentially no sugar (glucose) in their liver on autopsy, and likely died with hypoglycemia. Recently, the Boles laboratory tested the DNA in those babies, and found that they are 6 times more likely to have 16519T than are SIDS babies with normal liver sugar levels. Furthermore, babies with 3010A are more than 3 times more likely to die of the most common (sugar-normal) type of SIDS than are babies with the more-common 3010G. Thus, these mitochondrial genetic changes do not only predispose towards pain and fatigue, but towards the fatal, yet preventable, complication of SIDS as well.