Magnesium Research (1993) 6, 3, 297-298
Commentary on recent clinical advances:
Death from infancy to older age and marginal maternal
magnesium deficiency. How long should the follow-up of the
consequences of undernutrition in pregnancy be continued?
Jean Durlach
President de la SDRM (Hôpital Saint-Vincent-de-Paul,
Paris), 64 rue de Longchamp, F-92200 Neuilly/Seine, France
Key words: Magnesium deficiency, pregnancy,
birth weight, birth length, head circumference, sudden infant
death syndrome, cardiovascular risk factors, maternal
undernutrition.
Higher incidence rates of sudden infant death syndrome (SIDS)
have been observed in infants of diminished birth weight. Several
analytical studies, for example the NICHD cooperative
study1 controlling a variety of confounders of birth
size have estimated the likelihood of SIDS deaths in relation to
the four variables of birth size: birth weight, birth length,
head circumference and gestational age. SIDS may be associated
with symmetrical intrauterine growth retardation because of
reduction in both birth weight and length even after controlling
for gestational age and sex of the infant. This suggests that
mechanisms responsible for growth retardation in this situation
begin early in pregnancy1. Various subtle
morphological differences between SIDS and controls support the
notion of early intrauterine injury as playing some part in the
genesis of SIDS2.
Several English surveys have indicated that reduction in fetal
growth which begins early in gestation is followed by increased
mortality from cardiovascular disease in adult life. One of them,
concerning 1586 men born in a maternity hospital in Sheffield
between 1907 and 1925 showed that death rates from cardiovascular
diseases fell progressively with increasing weight, head
circumference and weight/length ponderal index at
birth3. In another one, dealing with 5694 men born in
Hertfordshire between 1911 and 1930, examination of men and women
showed that lower birth weight is associated with a higher
incidence of known risk factors for cardiovascular disease,
including raised blood pressure, plasma glucose and basal insulin
concentrations, plasma fibrinogen and factor VII
concentrations4. The studies in Preston have shown
that babies who have small head circumferences and are thin at
birth tend as adults to develop a "syndrome X": a combination of
hypertension, non-insulin dependent diabetes, disordered lipids,
hyperinsulinaemia, obesity and abdominal fatness5.
It has been argued that people whose growth has been impaired
in utero may continue to be exposed to an adverse
environment in infancy, childhood and adult life and it may be
this later environment that produces the effects being attributed
to programming. But the associations with cardiovascular risk
factors are independent of known influences in lifestyle: they
occur in each social class, and at each level of cigarette
smoking, alcohol consumption and obesity4.
Fetal growth can also be constrained by maternal size. But a
baby's birth measurements, however, are predictive of adult
disorders independent of maternal pelvic size3, 4.
These very interesting studies, mainly by the MRC
Environmental Epidemiology Unit of Southampton directed by D.J.P.
Barker, suggested that cardiovascular disease and non-insulin
dependent diabetes may begin early in gestation. Maternal
nutrition may have an important influence on programming of the
body structure and physiology. Persisting changes in the levels
of hormone secretion and in the sensitivity of tissue to them may
link fetal undernutrition with abnormal structure, function and
disease in life3-5.
Among the multiple variables of maternal undernutrition which
may induce frequently early symmetrical intrauterine growth
retardation, experimental and clinical data have highlighted the
importance of marginal magnesium deficiency2, 6-8.
Several prospective double-blind studies in Germany and in
Hungary on the effects of the control of chronic marginal
maternal magnesium deficiency by oral physiological magnesium
supplementation have shown their beneficial effects on all the
stigmata of diminished development of the baby at birth: such as
birth weight, crown-heel length, and head circumference2,
9. Therefore maternal magnesium intake appears to be one of
the factors of nutrition in pregnancy which induces reduced fetal
growth and may have an influence during the entire life on
programming.
The classical studies of magnesium supplementation only
analyse its effects on the mother, the fetus and the neonate at
birth9. The main consequence of the
magnesium-dependent thermal dysregulation theory of SIDS is to
follow up the baby over the first year in order to check the
validity of this important hypothesis2. But now--after
the seminal epidemiological studies by Barker--the protocol of
the multicentre trials of maternal magnesium supplementation
should be followed up not only during the first year but
throughout life. This notion should be borne in mind during the
development of this protocol to get the best of it in the
future.
References
1. Van Belle, G., Hoffman, H. & Peterson, D. (1988):
Intra-uterine growth retardation and the sudden infant death
syndrome. In: Sudden infant death syndrome: risk factors and
basic mechanisms. eds. R.M. Harper & H.J. Hoffman, pp.
203-219. New York: PMA Publishing Corporation.
2. Durlach, J., Durlach, V., Rayssiguier, Y., Ricquier, D.,
Goubern, M., Bertin, R., Bara, M., Guiet-Bara, A., Olive, G.
& Mettey, R. (1991): Magnesium and thermoregulation. I.
Newborn and infant. Is sudden infant death syndrome a
magnesium-dependent disease of the transition from chemical to
physical thermoregulation? Magnes. Res.
4, 137-152.
3. Barker, D.J.P., Osmond, C., Simmonds, S.J. & Wield,
G.A. (1993): The relation of small head circumference and
thinness at birth to death from cardiovascular disease in adult
life. BMJ 306, 422-426.
4. Barker, D.J.P., Gluckman, P.D., Godfrey, K.M., Harding,
J.E., Owens, J.A. & Robinson, J.S. (1993): Fetal nutrition
and cardiovascular disease in adult life. Lancet
341, 938-941.
5. Barker, D.J.P., Hales, C.N., Osmond, C., Phipps, K. &
Clark, P.M.S. (1993): Type 2 (non-insulin dependent) diabetes
mellitus, hypertension and hyperlipemia (syndrome X): relation to
reduced fetal growth. Diabetologia 36,
62-67.
6. Kubena, K.S. & Durlach, J. (1990): Historical review of
the effects of marginal intake of magnesium in chronic
experimental magnesium deficiency. Magnes. Res.
3, 219-226.
7. Durlach, J. (1989): Recommended dietary amounts of
magnesium: Mg RDA. Magnes. Res. 2,
195-203.
8. Durlach, J. & Mareschi, J.P. (1991): Recommended
dietary amounts for magnesium: updated European Consensus and
future prospects. In: Magnesium: a relevant ion, eds. B.
Lasserre & J. Durlach, pp. 39-49, London: John Libbey.
9. Spatling, L., Disch, G. & Classen, H.-G. (1989):
Magnesium in pregnant women and the newborn. Magnes.
Res. 2, 271-280.
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