The apparent impact of gestational magnesium (Mg) deficiency on the sudden infant death syndrome (SIDS).
Reports of studies in humans as well as data from several animal models show the importance of maternal dietary magnesium for the growth, development and survival of offspring. Published findings in mothers of victims of sudden infant death syndrome (SIDS) and in the SIDS victims are compared with characteristics of magnesium deficiency in humans and animals. Observations concerning the level of magnesium in traditional diets of selected ethnic groups with the highest or lowest rates of SIDS appear to confirm the importance of magnesium in protecting the offspring from sudden death. Ethnic groups with low SIDS rates at or below 1.2 per 1000 live births have rich dietary sources of magnesium, while those with SIDS rates exceeding 5.0 typically have magnesium-poor diets. Factors other than dietary magnesium are considered. Rat pups born and suckled by magnesium-sufficient dams have superior growth, development and survival, while those of deficient dams are feeble with impaired growth and development and have high perinatal mortality. In conclusion, these observations show that gestational magnesium deficiency results in suboptimal growth and development, with reduced survival of the offspring. Although the experimental data are compatible with a role for magnesium deficiency in SIDS, the cause of SIDS remains unknown and must be proved by appropriate biochemical analysis of tissue from SIDS infants compared with well-matched controls.
Caddell
J L
JL
Department of Pediatrics, Thomas Jefferson University, Philadelphia, PA 19107-5083, USA.
D000818:Animals; D004032:Diet; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008275:Magnesium Deficiency / Q000150:complications*; D009747:Nutritional Physiological Phenomena; D011247:Pregnancy; D011248:Pregnancy Complications / Q000378:metabolism*; D011256:Pregnancy Outcome; D051381:Rats; D013398:Sudden Infant Death / Q000209:etiology*