European Journal of Obstetrics & Gynecology and Reproductive Biology 162 (2012) 125–130

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European Journal of Obstetrics & Gynecology and

Reproductive Biology
journal homepage: www.elsevier.com/locate/ejogrb

Review

Prediction and prevention of the macrosomic fetus

Jennifer M. Walsh *, Fionnuala M. McAuliffe
UCD Obstetrics and Gynaecology, School of Medicine and Medical Science, University College Dublin, National Maternity Hospital, Dublin, Ireland

A R T I C L E I N F O A B S T R A C T

Article history: Fetal macrosomia is associated with significant maternal and neonatal morbidity. In the long term,
Received 4 November 2011 infants who are large for gestational age are more likely than other infants to be obese in childhood,
Received in revised form 27 February 2012 adolescence and early adulthood, and are inherently at higher risk of cardiovascular and metabolic
Accepted 2 March 2012
complications in adulthood. With over one billion adults in the world now overweight and more than 600
million clinically obese, preventing the vicious cycle effect of fetal macrosomia and childhood obesity is
Keywords: an increasingly pertinent issue.
Macrosomia
Fetal growth is determined by a complex interplay of various genetic and environmental influences.
Prediction
Consequently the prediction of pregnancies at risk of pathological overgrowth is difficult. Many risk
Prevention
factors for fetal macrosomia, such as maternal obesity and advanced maternal age, are also conversely
associated with intrauterine growth restriction. Sonographic detection of fetal macrosomia is notoriously
fraught with difficulties, with dozens of formulas for estimated fetal weight proposed but few with
sufficient sensitivity to alter clinical practice. This calls into question policies of elective delivery based on
projected estimated fetal weight cut-offs alone. More recently the identification of markers of fetal
adiposity and maternal serum biomarkers are being investigated to improve the antenatal detection of
the large for gestational age fetus.
Prevention of fetal macrosomia is entirely dependent upon correct identification of those at risk.
Maternal weight, gestational weight gain and glycaemic control are the risk factors for fetal macrosomia
that are most amenable to intervention, and have potential maternal health benefits beyond pregnancy
and childbirth. The ideal method of optimising maternal weight and glucose homeostasis is yet to be
elucidated, though a number of promising advances are recently being reported.
In this review we outline the contemporary evidence for the prediction and prevention of fetal
macrosomia, which is indeed a contemporary dilemma.
ß 2012 Elsevier Ireland Ltd. All rights reserved.

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 126
2. Prediction of fetal macrosomia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 126
2.1. Prediction based on risk factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 126
2.2. Prediction based on clinical findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127
2.3. Prediction based on ultrasound findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127
2.4. Prediction based on serum biomarkers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128
3. Prevention of fetal macrosomia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128
3.1. Exercise in pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128
3.2. Treatment and prevention of diabetes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128
3.3. Maternal diet . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129
4. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129

* Corresponding author. Tel.: +353 0 1 6373216.

E-mail address: jennifer.walsh@ucd.ie (J.M. Walsh).

0301-2115/$ – see front matter ß 2012 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.ejogrb.2012.03.005
126 J.M. Walsh, F.M. McAuliffe / European Journal of Obstetrics & Gynecology and Reproductive Biology 162 (2012) 125–130
1. Introduction
The large for gestational age fetus is predisposed to a variety of
adverse obstetric and neonatal outcomes, largely accounted for by
the excess risks associated with labour and delivery, including
shoulder dystocia and brachial plexus injury [1,2]. Delivery of a
large infant also significantly increases the risk of birth complica-
tions for the mother [3,4]. In the neonatal period, macrosomic
infants are predisposed to electrolyte and metabolic disturbances,
such as hypoglycaemia, hyperbilirubinaemia and hypomagnesae-
mia [5]. In the long term, infants that are at the highest end of the
distribution for weight or body mass index (BMI) are more likely
than other infants to be obese in childhood, adolescence, and early
adulthood [6], and are at risk of cardiovascular and metabolic
complications later in life [7,8].
Fetal macrosomia is varyingly defined as either an absolute
birthweight greater than 4000 g, 4500 g or 5000 g, or as a
customised birth weight centile of greater than the 90th, 95th
or 97th percentile for the infant’s gestational age. None of these
terms discriminates the fetus of abnormal body composition from
normal. Customised centiles based on individual fetal growth
potential are recognised to increase the likelihood of differentiat-
ing between physiological and pathological growth [9]. Birth
trauma rates for the macrosomic fetus appear to be more closely
related to absolute birthweight rather than birth weight centile,
though there is evidence for a strong correlation between fetal
macrosomia with a short maternal stature and the likelihood of
birth injury [10]. The metabolic consequences of macrosomia,
however, are more likely to be secondary to pathological
overgrowth and abnormal fat deposition in utero [11] than to
either absolute birthweight or birthweight centile.
With over one billion adults in the world now overweight and
more than 600 million clinically obese [12], methods to accurately
predict and ultimately prevent fetal macrosomia are now essential
to reduce this potential global health burden.
2. Prediction of fetal macrosomia
Prediction of fetal macrosomia is notoriously fraught with
difficulties and calls into question policies of elective delivery for
estimated fetal weight alone. Possible methods include identifica-
tion of those at risk, clinical examination, ultrasound assessment
and most recently the use of predictive biomarkers.
2.1. Prediction based on risk factors
A number of risk factors for macrosomia are unmodifiable.
These include parental height, parity, ethnicity, maternal age,
infant gender and previous delivery of a large for gestational age
infant. Macrosomia may also be secondary to genetic syndromes
which disrupt normal fetal growth regulation, such as the
Beckwith–Wiedemann or Perlmann syndromes [10].
Both maternal and paternal heights have been associated with
infant birthweight, though to a lesser extent with the latter [13].
There is a recognised association between advanced maternal age
and macrosomia [14]. An analysis of over 8 million births in the
United States from 1995 to 1997 by Boulet et al. [3] confirmed that
mothers of macrosomic infants were significantly more likely than
those of normal birth weight infants to be married and older (>35
years old), and less likely to be under 18 years old and primiparous.
Male fetuses during the third trimester have been reported to be
significantly heavier than females matched for gestational age [15]
with a rate of fetal weight gain 0.5 g/day greater than female
fetuses.
Women with a history of one macrosomic infant are at
significantly increased risk of delivering another macrosomic
infant in a subsequent pregnancy, with an odds ratio of 15.8 in one
study [16]. For women with two or more macrosomic infants, the
risk is even greater (OR 47.4). Overall, a first delivery of a
macrosomic infant weighing greater than 4500 g is associated with
a recurrence rate of 32%, compared to just 0.3% in those that deliver
a normal birthweight infant the first time [17] (Tables 1 and 2).
Potentially modifiable predictors of birthweight include ma-
ternal weight, gestational weight gain, gestational age at birth and
maternal glucose metabolism.
Maternal weight and maternal weight gain during pregnancy
exert an important influence on infant birth weight [18–20].
Increased maternal body mass index (BMI) confers an elevated risk
of delivering a heavier infant [21], while increasing maternal
weight gain during pregnancy has been shown to be independently
related to increasing infant birth weight [22,23]. Maternal weight
gain of more than 11 kg is strongly associated with birth of a large
for gestational age neonate [24]. A review by Siega-Riz et al. in
2009 [25] of all studies that examined the relationship between
gestational weight gain and large for gestational age babies
concluded that there is strong evidence to support associations
between excessive gestational weight gain and increased birth-
weight and fetal growth. Excessive interval pregnancy weight gain
has also been shown to be associated with an increased risk of
macrosomia and its inherent complications [26]. It has been shown
that women with lower weight gain in pregnancy deliver smaller
infants than women with higher gains [27].
The incidence of macrosomia increases as gestational age
advances. Early studies of intrauterine growth suggested that
normal fetal weight gain is curvilinear between 37 and 42 weeks
gestation, with fetal growth rates declining as gestation advances
[28,29]. The hypothesis for this decline in fetal growth rate was
that there was progressive uteroplacental insufficiency as a result
of placental aging. One may then assume that if placental function
remained adequate as gestational age advances that fetal growth
rate would be linear, and the post-dates fetus would be at
particular risk of fetal macrosomia. Indeed, in a number of studies
with strict exclusion criteria which eliminated pregnancies of
uncertain gestational age or those associated with adverse medical
or obstetric conditions this was found to be the case [15]. Despite
the association between post-dates pregnancies and increased
infant birthweight, no benefit from elective induction of labour or
caesarean delivery in non-diabetic pregnancies with suspected
fetal macrosomia has been established [30].
Altered maternal glucose homeostasis is perhaps the most
significant risk factor for fetal macrosomia and also one of the factors
most amenable to intervention. Glucose is the main energy substrate
for fetal growth [31]. Birthweights in infants of diabetic mothers are
increased, with up to 35% above the 95th percentile [32]. In terms of
predicting which infants of diabetic pregnancies are most at risk it
has been suggested that post-prandial, rather than fasting, glucose
concentrations are most predictive of subsequent birthweight [33].
The aim of management of diabetic pregnancies is to achieve
maternal glucose levels that are similar to a non-diabetic pregnant
population and in doing so achieve a similarly good obstetric
outcome. The majority of macrosomic infants, however, are born to
non-diabetic women. In 2008, a large prospective study of over
23,000 participants was published [34]. The Hyperglycemia and
Adverse Pregnancy Outcome (HAPO) study found strong, continuous
associations of maternal glucose levels at 24–32 weeks gestation,
below those diagnostic of diabetes, and a variety of adverse
pregnancy outcomes such as caesarean delivery, neonatal hypogly-
cemia, birthweight above the 90th centile, shoulder dystocia, birth
injury and pre-eclampsia. This large study, and a number that have
subsequently followed, support previous experimental evidence
that suggested a direct relationship between maternal glucose levels
and infant birth weight [35,36].
 J.M. Walsh, F.M. McAuliffe / European Journal of Obstetrics & Gynecology and Reproductive Biology 162 (2012) 125–130
Table 1
Prediction of fetal macrosomia.
Risk factor based prediction
Parental height Rice et al. [13]
Maternal age Spellacy et al. [14]
Infant gender Nahum et al. [15]
Previous delivery of a macrosomic infant Walsh et al. [16]
Mahony et al. [17]
Maternal weight and gestational weight gain Abrams et al. [18]
Frentzen et al. [19]
Johnson et al. [20]
Seidman et al. [21]
Selvin et al. [22]
Jensen et al. [23]
Bianco et al. [24]
Siega-Riz et al. [25]
Walsh et al. [26]
Shapiro et al. [27]
Gestational age Nahum et al. [15]
Maternal glucose metabolism Moses et al. [31]
Hawthorne et al. [32]
de Veciana et al. [33]
HAPO Study Cooperative
Research Group [34]
Clapp et al. [35]
Walsh et al. [36]
Clinical findings
Abdominal palpation Hall et al. [37]
Symphysiofundal height assessment Rosenberg et al. [41]
Belizán et al. [42]
Gardosi et al. [43]
Neilson [44]
Kayem et al. [45]
Wikström et al. [46]
Ultrasound findings Melamed et al. [47]
Chauhan et al. [48]
Hoopmann et al. [49]
Melamed et al. [50]
Hart et al. [52]
Nahum et al. [53]
Chauhan et al. [54]
Higgins et al. [55]
Petrikovsky et al. [56]
Serum biomarkers Lauszus et al. [59]
Goetzinger et al. [60]
Poon et al. [61]
Nanda et al. [62]
A summary of current literature relating to prediction of fetal macrosomia.
2.2. Prediction based on clinical findings
Clinical estimation of fetal weight has been found in a number
of studies to be poor, with detection rates of just 40–50% [37,38], as
has maternal estimated fetal weight estimation [39]. Methods of
clinical estimation of fetal size include abdominal palpation and
symphysis-fundal height measurement. In many settings, sym-
physis-fundal height measurement has replaced clinical assess-
ment of fetal size by abdominal palpation because the latter has
been reported to perform poorly, with detection rates between 30%
and 50% [40]. Assessment of symphysis-fundal height measure-
ment has been reported to perform somewhat better [41,42];
furthermore it has been suggested that serial measurement of
fundal height plotted on customised charts leads to increased
antenatal detection of small and large babies [43]. A Cochrane
review concluded that there is not enough evidence to evaluate the
use of symphysis-fundal height measurements during antenatal
care, though the author did conclude that it would seem unwise to
abandon the use of symphysis-fundal height measurement unless
a large trial suggests that it is unhelpful [44]. Sonographic
assessment of fetal size is likely superior to clinical estimation
[45] but it appears that macrosomia detection rates can be
improved by a combination of the two [46].
127
2.3. Prediction based on ultrasound findings
There is much debate in the literature as to which sonographic
estimated fetal weight formulation best predicts the macrosomic
fetus. Commonly used weight formulas are associated with very
large deviations when used in the macrosomic fetus [47]. This is
partly because these formulas were derived from heterogeneous
groups and were not specifically designed for assessing fetal
weight at the upper end of the weight scale. Chauhan et al. in 2005
reviewed 20 articles that calculated the sensitivity and specificity
of sonographic estimated fetal weight of >4000 g to accurately
identify a macrosomic fetus [48]. The authors found that the post-
test probability of sonographic estimated fetal weight of >4000 g
to identify a macrosomic newborn varied widely, from 15% to 79%.
They found that neither the type of regression equation used in the
estimated fetal weight formula, the time interval between
ultrasound and delivery, nor the experience of the sonographer
influenced the accuracy.
Hoopmann et al. compared the accuracy of 36 commonly used
weight estimation formulas in macrosomic fetuses [49]. They
concluded that though some formulas showed advantages as far as
mean and absolute percentage errors were concerned, none
reached a detection rate for the macrosomic fetus that could lead
to a clinical recommendation. Melamed et al. compared the
accuracy of 21 sonographic fetal weight-estimation models and
abdominal circumference (AC) as a single measure for the
prediction of fetal macrosomia and found that models based on
three or four biometric indices appeared to be more accurate for
the diagnosis of fetal macrosomia than models based on only two
indices or on AC as a single measure [50]. Pinette et al. examined
975 fetuses that had estimation of fetal weight by ultrasonography
within 1 week before birth, and concluded that using either the
mean value of multiple formulas or the Hadlock BPD/FL/AC
formula provided the best estimate of true weight without a trend
in either over- or under-estimation [51].
A number of authors have developed specific formulas for
estimating the weight of the macrosomic fetus taking both fetal
biometry and maternal weight into account and reported
improved macrosomia detection rates [52,53].
More recently measurements of various markers of fetal
adiposity have been assessed in terms of more accurately
predicting fetal size. These include fetal upper arm or thigh
subcutaneous tissue, upper arm soft tissue thickness, fetal cheek-
to-cheek diameter and fetal anterior abdominal wall width (AAW).
Chauhan et al. conducted a comparison of five new estimation
techniques that involve measurements of soft tissue for identifying
newborns with birth weights of at least 4000 g [54]. Three of the
five newer methods (upper arm or thigh subcutaneous tissue and
ratio of thigh subcutaneous tissue to femur length (FL)) were found
to be poor diagnostic tests, whilst neither upper arm soft tissue
thickness nor cheek-to-cheek diameter were significantly better
than clinical predictions for detecting macrosomic fetuses.
Assessment of fetal anterior abdominal wall width has yielded
more promising results. In diabetic pregnancies, Higgins et al.
reported that the use of a raised AAW measurement better
predicted macrosomia than using AC alone [55], while Petrikovsky
et al. in a non-diabetic population found measurement of the
subcutaneous tissue thickness of the fetal abdomen was useful for
ruling out macrosomia [56]. The use of 3-dimensional volume-
based estimated fetal weight has recently been reported to more
accurately reflect neonatal fat mass and subsequent birthweight
when compared to traditional 2-dimensional sonographically
estimated fetal weight [57].
It is clear that further, larger studies are needed before
assessment of fetal adiposity can reliably predict subsequent
birthweight. Assessment of fetal adiposity may however play an
128 J.M. Walsh, F.M. McAuliffe / European Journal of Obstetrics & Gynecology and Reproductive Biology 162 (2012) 125–130

Table 2
Prevention of fetal macrosomia. 3. Prevention of fetal macrosomia
Exercise in pregnancy Committee on Obstetric Practice [63]
Royal College of Obstetricians and
Despite the limitations of macrosomia prediction as outlined
Gynaecologists [64] above, there is a clear need for effective and safe strategies to
Walsh et al. [65] reduce the incidence in at-risk populations.
Macera et al. [66] Maternal weight, gestational weight gain and glycaemic control
Bell et al. [67]
are the risk factors for fetal macrosomia that are most amenable to
Goodwin et al. [68]
Owe et al. [69] intervention, and that should be targeted for the primary
de Veciana et al. [33] prevention of the implications of fetal macrosomia for pregnancy
Treatment and Murphy et al. [70] and beyond. Exercise, healthy diet and lifestyle modifications
prevention of diabetes Landon et al. [71]
should be recommended to all identified as higher risk. Pre-
Dhulkotia et al. [72]
Rowan et al. [73]
pregnancy counselling and public health initiatives should stress
Khattab et al. [74] the importance of attaining a healthy weight prior to pregnancy
Glueck et al. [75] and the avoidance of excessive gestational weight gain following
Maternal diet HAPO Study Cooperative conception.
Research Group [34]
Walsh et al. [36]
Jenkins et al. [76] 3.1. Exercise in pregnancy
Fraser et al. [77]
NICE Public Health Guidance [78] Both the American College of Obstetricians and Gynecologists
Institute of Medicine [79] (ACOG) and the Royal College of Obstetricians and Gynecologists
Dodd et al. [80]
Walsh et al. [81]
(RCOG) recommend 30 min of daily moderate-intensity physical
Luoto et al. [82] activity for pregnant women [63,64] yet only a small proportion of
healthy women are meeting current recommendations for exercise
A summary of current literature relating to prevention of fetal macrosomia.
in pregnancy [65]. Moreover, the proportion of the general
population who exercise is larger than that of women who
exercise during pregnancy, indicating that women who exercise
additional role in identifying the fetus that is normally, constitu- regularly outside of pregnancy curtail or cease physical activity
tionally large for gestational age from the fetus that is patholog- prenatally [66]. One possible explanation for this is the perception
ically overgrown, and therefore, presumably, at higher risk of that exercise in pregnancy is potentially harmful — a belief that
metabolic complications in later life [58]. may be held by healthcare professionals as well as pregnant
Any ultrasound estimation of fetal weight is also subject to the women. Vigorous exercise during pregnancy has been linked to
limitations of sonographer training, imaging quality and maternal preterm birth and low birth weight, but moderate or mild exertion
adiposity. has not [67]. Reported benefits of exercise in pregnancy include a
reduced risk of pre-eclampsia and gestational diabetes, less
2.4. Prediction based on serum biomarkers gestational weight gain, and fewer somatic complaints (including
insomnia and low mood) [68]. Regular exercise during pregnancy
The discovery of a simple, sensitive and specific maternal serum reduces by 23–28% the odds of giving birth to newborns with
biomarker for future macrosomia risk could potentially allow excessive birth weight [69]. Overall, the benefits of exercise in
prediction of birthweight prior to excess intrauterine growth pregnancy outweigh the risks, and there are implications of a
occurring, and therefore allow pregnancy interventions in at-risk sedentary lifestyle for both pregnancy and later life. Pregnancy is
groups. no longer considered a period of confinement and may even
In diabetic pregnancies, increasing levels of IGF-I and -II have present an opportunity for lifestyle modification, because most
been found to be associated with birthweight, with higher levels of women are motivated to have healthy infants. Obstetricians,
IGF-I and -II in those with higher birthweight ratios [59]. general practitioners and other healthcare professionals should be
Goetzinger in 2009 investigated first-trimester analytes and found informed about the benefits of physical activity in pregnancy and
that low pregnancy-associated plasma protein A (PAPP-A) and high encouraged to educate women about its safety to them and their
free beta-human chorionic gonadotropin (b-hCG) levels are baby.
associated with a small-for-gestational-age growth pattern, but
that neither PAPP-A nor free b-hCG levels were associated with an 3.2. Treatment and prevention of diabetes
increased risk of large-for-gestational-age infants [60].
Much work on early prediction of subsequent macrosomia from The benefit of optimising blood sugars in pre-existing and
first trimester screening results have been carried out by established gestational diabetic pregnancies is clear. Post-prandial,
Nicolaides et al. This group reported a significant improvement rather than fasting, glucose concentrations are most predictive of
in the prediction of macrosomia provided by maternal factors by subsequent birthweight [33] and continuous glucose monitoring
the addition of fetal NT, free b-hCG and PAPP-A, albeit still during pregnancy is associated with improved glycaemic control in
relatively low overall (34.4 vs. 33.1% at a false-positive rate of 10%) the third trimester, as well as lower birth weight and a reduced risk
[61]. of macrosomia [70].
Additionally, maternal serum adiponectin at 11–13 weeks has The results of a multicenter, randomised trial of treatment for
been identified as a useful biomarker for early prediction of mild gestational diabetes concluded that although treatment did
macrosomia, increasing the detection from 34.6% with maternal not significantly reduce the frequency of a composite outcome
characteristics and obstetric history alone to 38.2% with the that included stillbirth or perinatal death, it did reduce the risk of
addition of serum adiponectin [62]. fetal overgrowth [71]. Oral hypoglycaemic agents are now being
Though this technology is still in relative infancy it holds used with greater frequency in the treatment of gestational
perhaps the most promise for early prediction and therefore diabetes, with good results [72]. Metformin in particular is
potential prevention of fetal macrosomia and its inherent increasingly used as a first-line medical treatment for gestational
implications. diabetes [73].
 J.M. Walsh, F.M. McAuliffe / European Journal of Obstetrics & Gynecology and Reproductive Biology 162 (2012) 125–130
Primary prevention of gestational diabetes involves lifestyle
and dietary modifications to optimise maternal BMI pre-pregnan-
cy. A number of studies have also evaluated the role of metformin
in preventing gestational diabetes in at-risk populations, with
promising results [74,75].
3.3. Maternal diet
There is good evidence that maternal diet plays a role in fetal
growth. There is evidence of a direct relationship between maternal
blood glucose levels during pregnancy and fetal growth and size at
birth, even when maternal blood glucose levels are within their
normal range [34,35]. Thus, maintaining blood glucose concentra-
tions within normal parameters during pregnancy may reduce the
incidence of fetal macrosomia. Maternal diet, and particularly its
carbohydrate (CHO) type and content, influences maternal blood
glucose concentrations. However, different CHO foods produce
different glycaemic responses. The glycaemic index (GI) was
conceived by Jenkins in 1981 as a method for assessing the glycaemic
responses of different carbohydrates [76]. Pregnancy is a condition
where the GI may be of particular relevance, as glucose is the primary
fuel for fetal growth. It has been shown that a low glycaemic diet
blunts the mid and late pregnancy increase in insulin resistance
typically seen in Westernised societies [77]. These studies suggest
that the loss of insulin sensitivity, which is typical of Western women
in the third trimester of pregnancy and is considered to be
physiological, may be diet-induced. Eating primarily high glycaemic
carbohydrate results in foeto-placental overgrowth, excessive
maternal weight gain and predisposition to fetal macrosomia, while
intake of low-glycaemic carbohydrate predisposes to normal infant
birth weight and normal maternal weight gain [35].
Gestational weight gain is associated with fetal macrosomia,
and it is notoriously difficult for mothers to regain their pre-
pregnancy weight following delivery. The current National
Institute for Health and Clinical Excellence (NICE) recommenda-
tion [78] that women not be weighed in pregnancy, and the lack of
clear guidance on what optimal gestational weight gain should be,
appear contrary to the mounting body of evidence pointing toward
a detrimental effect of excess gestational weight gain for both
mother and baby [25]. The Institute of Medicine has provided clear
guidance on optimal gestational weight gain according to maternal
early pregnancy BMI [79]. In the light of the known association
between excessive gestational weight gain and interval pregnancy
weight gain on obstetric outcome, clear guidance for women,
particularly for those in at-risk groups, is needed. It would seem
that both providing this guidance and assessing its effects are
impossible if women are not weighed during pregnancy and
gestational weight gain calculated.
Targeting the maternal obesity epidemic would appear to be
pivotal in breaking the escalating rates of both maternal and
childhood obesity and public health initiatives should be clearly
focused toward advocating a healthy lifestyle in pregnancy and
beyond.
A recent systematic review of antenatal interventions for
overweight or obese pregnant women concluded that the effect of
providing an antenatal dietary intervention for overweight or obese
pregnant women on maternal and infant health outcomes remains
unclear [80]. A randomised control trial assessing the impact of a low
GI diet in the prevention of recurrence of macrosomia is awaited [81],
as is a cluster-randomised controlled trial of exercise and dietary
intervention to prevent gestational diabetes [82].
4. Conclusion
In conclusion, the macrosomic infant poses significant chal-
lenges to obstetric care and can have potential implications for
129
both mother and baby long after labour and delivery. Antenatal
detection of the macrosomic fetus is inadequate but advances are
being made, both in improvements to estimated fetal weight
formulas and in first-trimester prediction. Maternal weight,
gestational weight gain and glucose homeostasis are targets for
primary prevention of fetal overgrowth and its implications.
Further work is needed to interrogate the relationship between
maternal and fetal metabolic milieus to understand clearly the
pathways and metabolic mechanisms underlying fetal over-
growth. Effective public health strategies are required to recognise
and combat the incidence of fetal macrosomia as a significant
precursor of childhood obesity and adult ill-health.
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