Sudden infant death syndrome SIDS is not fully understood. A number of theories have been presented to explain this unfortunate and devastating event, some of which involve nutritional mechanisms. In 1980, a theory was presented by Johnson and his coworkers that suggested that SIDS was possibly related to changes in the fatty acid metabolism of the liver. In particular, fatty acid accumulation in the liver of infants who had died of SIDS produced fatty livers. The researchers also noted that infants dying of SIDS has lower hepatic biotin levels compared to control infants. Similarities between the lower hepatic biotin levels in human infants and an increase risk of death were made with broiler chickens that showed similar fat accumulation in their liver and similar higher mortality when deprived of biotin. In such birds, the levels of palmitoleic acid (PA, C16:1 (n-7))) was elevated suggesting considerable changes to fatty acid metabolism. In fact, PA is a marker in humans for increased de novo lipogenesis, and accumulation is associated with abdominal obesity and non-alcoholic fatty liver in adult humans.
In addition, the concentrations of essential fatty acids in infants who died of SIDS has been found to be modified. Changes to normal arachidonic acid (AA, C20:4 (n-6)), linoleic acid (LA, C18:2 (n-6)), gamma linolenic acid (GLA, C18:3 (n-6)) and dihomo gamma linolenic acid (DGLA, C20:3 (n-6)) have been found. Suggestions that the omega 6 fatty acid metabolism in SIDS infants may be aberrant is of interest because GLA and DGLA are the parents of the series 1 eicosanoids which are known to have anti-inflammatory effects. Arachidonic acid in turn is a parent compound for the series 2 eicosanoids which are involved in the formation of inflammation in tissues. Higher levels of AA and lower levels of GLA and DGLA may therefore promote inflammation and disease, and ultimately lead to premature death. That eicosanoids and their ratios are involved in the regulation of respiration is interesting, and in particular DGLA and the series 1 eicosanoids and AA are known to play a pivotal role in this function. That respiratory failure is a possible mechanism for death in SIDS can therefore be explained.
Fatty acid analyses have been performed on the livers of SIDS infants under 1 years old compared to infants who died of other causes1. Significant differences in the fatty acid composition of SIDS infants were found when compared to the control infants, but only in infants of less than 6 months old. However, as most cases of SIDS occurs in infants under 6 months of ages, this is of nutritional interest. In particular, concentrations of DGLA were lower in the SIDS infants when compared to controls. This suggests that there may have been changes to the production of the beneficial anti-inflammatory series 1 eicosanoids in these infants. In addition, palmitoleic acid (PA, C16:1 (n-7)), palmitic acid (PA, C16:0) and oleic acid (OA, C18:1 (n-9)) were positively correlated with the fat content of the liver, while polyunsaturated fatty acids were negatively correlated with the fat content. Polyunsaturated fatty acids are preferentially used structurally in phospholipids whereas PA, OA and POA are preferentially incorporated into triglycerides, hence the association of the latter with liver fat content.
Because the infant is reliant on breast milk to obtain essential fatty acids in its early life, these changes to the fatty acid composition of the liver may reflect the fatty acid composition of the mother’s milk. Breast milk contains GLA and DGLA which may supply the infant with essential fatty acids required for correct growth. In contrast. cow’s milk contains linoleic acid but neither GLA nor DGLA. Theoretically LA can be converted to GLA and then DGLA via a series of desaturase and elongase enzymes. However, delta 5-desaturase activity in humans is not good and so relying of LA for the production of the series 1 eicosanoids is problematic. Additionally, LA can be converted to the pro-inflammatory series 2 eicosanoids. Infants fed cow’s milk may therefore develop essential fatty acid deficiencies that affect the composition and health of the liver which leads to detrimental changes in fatty acid metabolism. The practice of including toxic fats such as hydrogenated and trans fatty acids in infant formula cow’s milk should also be questions as it is known that such fats interfere with the metabolism of essential fatty acids.
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