Obesity has long been
recognised as a risk
factor for
the development of variety of
life
threatening diseases; examples
include diabetes mellitus and cardio vascular disease.
In
particular, in
young women,
it is widely
thought to predispose towards impaired
glucose tolerance and gestational
diabetes. Obesity is not only common but it is
increasing
in prevalence
despite the efforts made by individuals and their health
advisors to avoid
it.
Identification
of
factors contributing
to obesity could be useful
in
planning
preventative
policies.
Many
women relate the onset of
their obesity
to one or more of their pregnancies. We
now know
that there is more
to obesity
than the actual amount of excess weight. The
adverse metabolic effects of obesity are proved
to be greater when excess
fat
deposition
is
central rather
than peripheral. The idea
that fat deposition may be
directed
to different body sites with
different effects on glucose tolerance and
insulin
levels,
is
a relatively new concept.
The majority of
investigators have focused only on the magnitude of weight changes
during
pregnancy and postpartum.
There is
not much
information with regard to the compartmental changes
in body composition
during and after delivery. Most
studies
in
the developed world show maternal net
fat gain accompanying pregnancy. The
extent to which such
fat gain
is physiological, and what
is its beneficial
effects
is
unknown.
It is therefore
important to study the impact of other
factors with possible
effects on
fetal growth and maternal
body composition. The present work examines
further
the question of
fat
storage
by means of a
longitudinal
study to establish
changes
in body fat
content
during normal pregnancy and postpartum and also
its
relationship to maternal glucose
tolerance,
fetal metabolism, new-born anthropometry
and
infant
growth.
For
this purpose, 123 women were recruited at their first
visit to Antenatal Clinics
of
the Northern General Hospital, from which 73 completed 3 visits during
pregnancy
and 46
participated
in the whole course of the study. Maternal
anthropometry and
body
composition were measured at 13 (5
-
15), 24 (23
-
32) and 36 (34
-
41) weeks
gestation during pregnancy and also 6 weeks and 6 months postpartum. Skinfold
thickness measurements and Bio-electrical Impedance were used to assess the changes
in body
composition during pregnancy and postpartum.
Glucose
tolerance tests were performed at 28-31 weeks gestation.
Insulin
and/or C-
peptide
levels were also collected at birth and assessed
later. Infant anthropometry
(weight, length and
head circumference) were measured at birth, 6 weeks and 6
months postpartum.
The
subjects were
divided into four groups of under-weight, normal weight, over-
weight and obese, based on their early pregnancy BMI. The
statistical analyses were
performed on the whole group and also the groups were then compared
for
the above
mentioned variables.
The
two methods
(Skinfold thickness measurements and Bio-electrical Impedance)
showed a reasonable agreement
in
predicting the fat
changes during
pregnancy. A
considerable variation was observed,
however, between
the two methods
in
the
results
of changes
from early pregnancy
to postpartum. Therefore, direct interpretation
of
skinfold thickness (which was consistent with the converted version of
it
to fat mass)
was alone chosen
to derive the conclusions During
pregnancy, a
formula which
is
corrected
for hydration
changes during
gestation, was used to convert skinfold
thicknesses to fat mass. The
results confirmed
that a substantial net gain of
fat was made during pregnancy of which a significant
amount was still retained at 6 month postpartum. Maternal weight
increased (10.87
kg ± 4.67), but it
reverted
to the early pregnancy values by 6 months postpartum. The
rate of
fat
and weight changes was significantly higher in
the first half
of pregnancy
compared to later. The observed changes
in maternal weight and
fat mass, during
pregnancy were not significantly
different between the BMI groups
(normal weight,
over-weight and obese group). At the postpartum period, the obese group retained
more of the net
fat gain than the other
two groups. A state of redistribution of
fat
tissue was observed
in the subjects
in particular
in the obese group who had
a
tendency towards central
fat
retention.
Gestational fat gain was not directly
related
to infant birth weight.
In
this well
nourished population, maternal early pregnancy
lean body mass
(LBM) was the most
significant predictor of
infant birth weight.
There was a positive correlation
between maternal BMI and cord
insulin (r=0.44,
p=0.002) and/or C-peptide (r=0.33, p=0.008).
In addition higher levels
of
insulin
were observed
in large for gestational age
(LGA) babies in
comparison with the
average
for gestational age
(AGA) babies. These observations might have
an
important impact on the care of overweight women.
It may be
that
reduction of
maternal BMI in the prepregnancy period
in
the obese women would reduce the risk
of gestational diabetes and also the rate of
fetal hyperinsulinemia
and macrosomia.
Further investigation on
this hypothesis is needed.
In
summary; obese women
had significantly heavier babies
than the normal weight
women. Maternal fasting glucose was significantly correlated to infant birth weight.
On
the other hand, maternal
fasting glucose and the level
of
fetal insulinisation
was
significantly associated with maternal early pregnancy BMI. This is likely
to be a
metabolic effect operating
throughout gestation. What we can suggest
is
that
,
in
the
studies of maternal glucose metabolism and
fetal
growth, the confounding effects of
maternal BMI
should
be seriously considered