New data on the importance of gestational Mg deficiency

Abstract

Chronic primary Mg deficiency is frequent. Around 20% of the population consumes less than two-thirds of the RDA for Mg, in both genders and in women particularly: for example, in France, 23% of women and 18% of men. Primary Mg deficiency may occur in fertile women. Gestational Mg deficiency is able to induce maternal, fetal, and pediatric consequences which might last throughout life. Experimental studies of gestational Mg deficiency show that Mg deficiency during pregnancy may have marked effects on the processes of parturition and of postuterine involution. It may interfere with fetal growth and development from teratogenic effects to morbidity: i.e. hematological effects and disturbances in temperature regulation. Clinical studies on the consequences of maternal primary Mg deficiency in women have been insufficiently investigated. To check the validity of the role of this frequent gestational Mg deficiency, the protocol of a long term multicentric placebo controlled prospective study on the effects of maternal nutritional Mg supplementation on lethality and morbidity in fetus, neonates, infants, children and adults should be carried out not only during pregnancy and the first year of life, but throughout life. Two clinical forms of chronic gestational Mg deficiency in women have been stressed: Premature labor when chronic maternal Mg deficiency is involved in uterine hyperexcitability, Sudden Infant Death Syndrome (SIDS) when it is caused by either simple Mg deficiency or various forms of Mg depletion. Nutritional Mg treatment of premature labor. If gestational Mg deficiency is the only cause for uterine overactivity, nutritional Mg supplementation constitutes the etiopathogenic atoxic tocolytic treatment. But although it is an adjuvant factor in premature labor, it is only a useful accessory treatment, devoid of toxicity but which increases the effectiveness and safety of the associated tocolytic drugs such as beta-2 mimetics. SIDS due to gestational Mg deficit: Mg deficiency or various forms of Mg depletion. SIDS may be caused by the fetal consequences of maternal Mg deficiency through an impaired control of Brown Adipose Tissue (BAT) thermoregulation, mechanisms leading to a modified temperature set point. SIDS may result from dysthermias: hypo- or hyperthermic forms. A possible prevention could rest on simple maternal nutritional Mg supplementation. Various stresses in pregnant women or in the infant may transform a simple Mg deficiency into Mg depletion: stress in baby care such as bedding in prone position, environmental factors such as parental smoking, but the role of chronopathological stress particularly appears to be too often neglected as it constitutes a clinical form of primary hypofunction of the biological clock [with its anatomical and clinical stigma such as reduced production of melatonin (MT) and of its urinary metabolite: 6 Sulfatoxy-Melatonin (6 SMT)]. SIDS might be linked to an impaired maturation of both the photoneuroendocrine system and BAT. A preventive treatment of this form of SIDS should associate atoxic nutritional Mg therapy for pregnant women with total light deprivation at night for the infant. The place of Mg therapy for the infant and of MT, L Tryptophan and taurine is uncertain for the moment.