Obesity and pregnancy mechanisms

Obesity and pregnancy: mechanisms
of short term and long term adverse
consequences for mother and child
Patrick M Catalano,1 2 Kartik Shankar3 4
1Department of Obstetrics
and Gynecology, Center for
Reproductive Health/MetroHealth
Medical Center, Cleveland, Ohio,
USA
2Case Western Reserve University,
Cleveland, Ohio, USA
3Arkansas Children’s Nutrition
Center, University of Arkansas
for Medical Sciences, Little Rock,
Arkansas, USA
4Department of Pediatrics,
University of Arkansas for Medical
Sciences, Little Rock, Arkansas, USA
Correspondence to: P M Catalano
[email protected]
Cite this as: BMJ 2017;360:j1
doi: 10.1136/bmj.j1
Introduction
Obesity is the most common problem in obstetrics that
affects both the mother and her offspring.1 It causes
short term and long term problems for the mother, such
as increasing her risk of gestational diabetes (GDM) and
pre-eclampsia.2 Because obese women are more likely to
have excessive gestational weight gain (GWG),3 this further
increases the risk of developing the metabolic syndrome in
later life. The offspring have an increased risk of obstetric
morbidity and mortality,4 and, consistent with the developmental
origins of health and disease, a long term risk of
childhood obesity and metabolic dysfunction.5
Options for the management of obesity in non-pregnant
women include lifestyle interventions, drugs to achieve
weight loss, and, because of sustained benefits, bariatric
bypass surgery. During pregnancy anti-obesity drugs
and bariatric surgery are not options. Unfortunately, a
large number of randomized controlled trials (RCTs) have
shown that lifestyle interventions have limited success
in decreasing excessive GWG or improving maternal or
neonatal short term perinatal outcomes.6
ABSTRACT
Obesity is the most common medical condition in women of reproductive age.
Obesity during pregnancy has short term and long term adverse consequences
for both mother and child. Obesity causes problems with infertility, and in early
gestation it causes spontaneous pregnancy loss and congenital anomalies.
Metabolically, obese women have increased insulin resistance in early pregnancy,
which becomes manifest clinically in late gestation as glucose intolerance and
fetal overgrowth. At term, the risk of cesarean delivery and wound complications
is increased. Postpartum, obese women have an increased risk of venous
thromboembolism, depression, and difficulty with breast feeding. Because
50-60% of overweight or obese women gain more than recommended by
Institute of Medicine gestational weight guidelines, postpartum weight retention
increases future cardiometabolic risks and prepregnancy obesity in subsequent
pregnancies. Neonates of obese women have increased body fat at birth, which
increases the risk of childhood obesity. Although there is no unifying mechanism
responsible for the adverse perinatal outcomes associated with maternal obesity,
on the basis of the available data, increased prepregnancy maternal insulin
resistance and accompanying hyperinsulinemia, inflammation, and oxidative
stress seem to contribute to early placental and fetal dysfunction. We will review
the pathophysiology underlying these data and try to shed light on the specific
underlying mechanisms
BMJ: first published as 10.1136/bmj.j1 on 8 February 2017. Downloaded from http://www.bmj.com/ on 13 February 2021 at Medical Sciences Library Texas A & M University. Protected by copyright.
STATE OF THE ART REVIEW
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spontaneous abortion, congenital anomalies, stillbirth,
placenta, maternal metabolism, gestational diabetes and
hypertension, pre-eclampsia, gestational weight gain,
macrosomia, neonatal body composition, lactation, diet
composition, diet quality, lifestyle interventions, epigenetics,
and microbiome. We prioritized RCTs, metaanalyses,
longitudinal observational studies, and cohort
studies. We included only full text English language peer
reviewed publications. We reviewed Cochrane Reviews on
preconception lifestyle for people with infertility, interventions
for preventing excessive weight gain during
pregnancy, exercise in pregnant women for prevention of
GDM, and diet or exercise for weight reduction in women
after childbirth. We used clinical guidelines from the
American Congress of Obstetricians and Gynecologists
(ACOG), the Royal College of Obstetricians and Gynaecologists
(RCOG), the Royal Australian and New Zealand
College of Obstetricians and Gynaecologists (RANZCOG),
the Society of Obstetricians and Gynaecologists of Canada
(SOGC) and the Institute of Medicine (IOM) for gestational
weight guidelines in pregnancy. We prioritized the results
of guidelines in this review for quality according to the
method outlined by the US Preventive Services Task
Force.
Effects of maternal metabolism on fertility and
reproduction
Obesity and reproductive function
Obesity perturbs the hypothalamic-pituitary-ovarian axis
and overweight women display shorter luteal phases and
lower levels of follicle stimulating hormone, luteinizing
hormone, and progesterone.15 A study of more than
45 000 assisted reproductive embryo transfers showed
that a higher BMI correlated with a reduced likelihood
of successful pregnancy when autologous oocytes were
used, but not when oocytes from lean donors were used,
suggesting a direct effect of obesity on the oocyte.16
Obesity is also associated with changes in ovarian
granulosa cells and the follicular fluid surrounding
the oocyte. Differences in follicular fluid insulin, triglycerides,
free fatty acids, proinflammatory cytokines,
oxidized low density lipoprotein, and fatty acid composition
have been observed in obese women, suggesting
that numerous mechanisms probably contribute to disruptions
in oocyte development.17‑19 Data from women
undergoing in vitro fertilization (IVF) from a donated
oocyte have been used to isolate the role of the endometrium,
but results have been conflicting. A meta-analysis
of data from six centers found no difference in the rate of
pregnancy, implantation, or miscarriage between obese
versus non-obese women.20 A recent study of surrogate
pregnancies also indicated that increasing BMI of the surrogate
mother had no significant effect on IVF, embryo
transfer, or neonatal outcomes.21 However, another study
of 9587 women found that obesity in the recipient had
negative effects on implantation, pregnancy success, and
live births,22 suggesting that obesity significantly alters
endometrial gene expression in women during the luteal
phase.23 Thus, evidence suggests that both uterine and
ovarian changes associated with obesity contribute to
reproductive dysfunction.
pregnancy. Because of the differences in body composition
among various racial groups, WHO has discussed
using different criteria for the classification of obesity in
Asian women.9
The prevalence of obesity began to increase in the last
decades of the 20th century in developed countries. From
1999 to 2010, obesity increased from 28.4% to 34.0% in
women of reproductive age (20-39 years) in the United
States.10 According to the Centers for Disease Control and
Prevention, the prevalence of obesity in women of reproductive
age did not change significantly between 2003-
2004 and 2011-2012.11 However, 7.5% of women in this
age group have class III obesity or BMI greater than 40.1
Currently in the US, 31.9% of reproductive age women are
obese and 55.8% are overweight or obese, with a higher
prevalence in non-Hispanic black and Mexican American
women (table 2).1
The global age standardized mean BMI in women
increased from 22.1 (credible intervals 21.7 to 22.5) in
1975 to 24.4 (24.2 to 24.6) in 2014, with a doubling of
the prevalence of obesity between 1980 and 2008.12 In
2000, WHO noted that obesity “is now so common that it
is replacing the more traditional public health concerns,
including undernutrition and infectious disease, as one of
the most significant contributors to ill health.”7 In Europe,
WHO estimates that more than 50% of men and women
are overweight or obese and 23% of women are obese. In
South East Asia, 14% of the population are overweight
and 3% are obese.13 The prevalence of obesity in women
is double that of men in Africa and South East Asia.14 The
increase in obesity is not confined to adults—there have
been increases in obesity in children13 and significant
increases in birth weights among various populations.2
This review will discuss the potential mechanisms by
which maternal obesity in pregnancy propagates the
vicious cycle of obesity throughout the life course.
Sources and selection criteria
The references for this review were obtained from various
sources including PubMed and ClinicalTrials.gov.
We searched PubMed from 1990 to July 2016 using the
search terms pregnancy, obesity, overweight, fertility,
Table 1 | World Health Organization body mass index (BMI)
categories7
Category BMI*
Underweight Less than 18.5
Normal weight 18.5-24.9
Overweight 25.0-29.9
Obesity class I 30.0-34.9
Obesity class II 35.0-39.9
Obesity class III 40 or greater
Table 2 | Prevalence of obesity (measured by body mass index; BMI) by race or ethnicity in women
of reproductive age1
All race/ethnic
groups
Non-Hispanic
white
Non-Hispanic
black Hispanic Mexican-American
BMI ≥30
20-39 years 31.9 (28.6-35.5) 26.9 (23.0-31.3) 56.2 (44.3-67.5) 34.4 (30.9-38.2) 37.8 (33.2-42.7)
BMI ≥25
20-39 years 55.8 (49.6-61.9) 50.7 (43.1-58.2) 74.2 (65.9-81.1) 65.4 (59.9-70.5) 68.8 (62.1-74.8)
BMJ: first published as 10.1136/bmj.j1 on 8 February 2017. Downloaded from http://www.bmj.com/ on 13 February 2021 at Medical Sciences Library Texas A & M University. Protected by copyright.
STATE OF THE ART REVIEW
For personal use only 3 of 16
g; P=0.002),29 and placental weight has a stronger correlation
than maternal age, pre-pregnancy BMI, and GWG
with neonatal birth weight and fat mass.30 The maternal
metabolic environment affects early placental growth
and gene expression, as well as later placental function,
which become clinically manifest in late pregnancy.31 A
potential mechanism is that insulin receptors are more
abundant on the maternal trophoblast surface in early
gestation than in later gestation.32 The hyperinsulinemia
associated with obesity related insulin resistance results
in differential responses in placental trophoblasts.31
One study reported a 30-fold decrease in insulin sensitive
genes that regulate the cell cycle and cholesterol
homeostasis in placental villous tissue from obese
women during the first trimester. Maternal obesity, insulin
resistance, and hyperinsulinemia together impaired
global gene profiling related to mitochondrial dysfunction
and decreased energy metabolism.31 For example, the
maternal insulin secretory response in early pregnancy
is strongly correlated with placental weight and neonatal
adiposity at birth.33
The placentas of obese women at term are characterized
by an increase in total lipid content and an
accumulation of macrophages and proinflammatory
mediators compared with normal weight women.34 35 At
a molecular level, the placental transcriptome of obese
women with GDM shows activation of genes related to
lipid metabolism (fig 1).36 Pregravid obesity is associated
with a systemic low grade metabolic inflammatory
state and subclinical endotoxemia, both of which may
contribute to worsening of pregnancy associated insulin
resistance.37 Maternal obesity is associated with greater
placental cytokine expression and greater vessel muscularity
but little difference in other histological features
such as fibrin deposition or placental maturity.38 The precise
mechanisms underlying the inflammatory responses
and role in fetal growth, however, remain unclear.
The placenta has been hypothesized to function as
a “nutrient sensor,” whereby the placenta integrates
maternal and fetal nutritional cues, and through regulation
of nutrient sensing pathways attempts to match fetal
demand and maternal supply.39 In support of this model,
maternal obesity is associated with increased placental
expression of system A amino acid transporters 1 and 2
(SNAT1 and SNAT2) in conjunction with greater activity of
the mTOR (mechanistic target of rapamycin) and insulin
growth factor 1 (IGF-1) signaling pathways, which presumably
contribute to fetal overgrowth.40 By contrast, a
recent report found that maternal obesity decreased placental
taurine transporter activity in villous explants,
without changes in protein expression.41 Maternal obesity
and GDM also affect lipid transport across the placenta.
Placental expression of fatty acid binding protein
FABP4 and endothelial lipase is raised in obese women
with diabetes.42 43 Similarly, placentas from obese women
show increased lipid accumulation but lower concentrations
of FABP5 and uptake of omega-6 polyunsaturated
fatty acid (oleic acid).34‑45 Both increases and decreases in
the long chain polyunsaturated fatty acid (PUFA) transporter,
CD36, have been reported in placenta from obese
women.45 46 An important caveat of human placental
Increased risk of spontaneous abortion and congenital
anomalies
Overweight and obese women have an increased risk of
spontaneous miscarriage. A meta-analysis reported that
women with a BMI ≥25 had a higher risk of miscarriage
(odds ratio 1.67, 95% confidence interval 1.25 to 2.25).24
A subgroup analysis suggested a higher risk of miscarriage
after oocyte donation (1.52, 1.10 to 2.09) and induction of
ovulation (5.11, 1.76 to 14.83). An observational cohort
study of women with recurrent early pregnancy loss
reported that obese women had a 58% risk of euploid
miscarriage compared with 37% in non-obese women.25
Obese women are at increased risk of pregnancy
affected by congenital anomalies. A systematic review
and meta-analysis reported an increase in the following
congenital anomalies in the offspring of obese compared
with non-obese women: spina bifida (2.24, 1.86 to 2.69),
neural tube defects (1.87, 1.62 to 2.15), limb reduction
anomalies (1.34, 1.03 to 1.73), cardiovascular anomalies
(1.30, 1.12 to 1.51), and cleft lip and palate (1.20,
1.03 to 1.40).26 A prospective observational cohort study
reported a dose-response effect in relation to congenital
heart defects with increasing BMI (overweight: 1.15, 1.01
to 1.32; obese: 1.26, 1.09 to 1.44; and morbidly obese:
1.34, 1.04 to 1.43).27 Although maternal folate status and
glucose intolerance have been suggested, no definitive
mechanism has been identified.28
Placental changes associated with maternal obesity
The placentas of obese women are significantly heavier at
birth (mean 693 (standard deviation 184) g v 614 (152)
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Fig 1 | Differential expression of placental metabolic genes in lean women with type 1 diabetes
and obese women with gestational diabetes (gene expression increases as the color changes
from blue (downregulated) to red (upregulated). Unsupervised hierarchical clustering of
metabolic genes that are modified in the placenta of obese women with gestational diabetes
(GDM) and lean women with type 1 diabetes (type 1 DM). When the placental transcriptome at
term was compared between lean women with type 1 DM and obese women with GDM, genes
related to lipid metabolism were preferentially activated in obese women with GDM. Eleven
genes related to lipid transport and activation and seven genes related to lipid metabolism
were enhanced36
BMJ: first published as 10.1136/bmj.j1 on 8 February 2017. Downloaded from http://www.bmj.com/ on 13 February 2021 at Medical Sciences Library Texas A & M University. Protected by copyright.
STATE OF THE ART REVIEW
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cental size in early pregnancy is strongly correlated with
subsequent fetal adiposity at birth.33 The inflammatory
milieu of late pregnancy may be an important factor
affecting maternal insulin resistance.48
Differences in maternal metabolism in obese and normal
weight women
Pregnancy is a unique metabolic condition because of
the changes in maternal metabolism needed to provide
for fetal growth and increased maternal energy requirements.
Insulin sensitivity decreases by 40-50% during
the course of pregnancy but significantly improves within
days of delivery.49 50 The following data come from a secondary
analysis of the longitudinal changes in metabolism
in a small number of lean (n=6) and obese (n=10)
otherwise healthy women before a planned pregnancy
and during early and late gestation.51‑53
Lean and fat mass increased significantly in both lean
and obese women but the increase in fat mass was greater
in lean women (fig 2). Although there was a significant
23% increase in resting energy expenditure, over time
there was no significant difference between groups. Basal
carbohydrate oxidation increased 68% over time and was
greater in obese women.
There was a 40% decrease in insulin sensitivity in
lean and obese women over time and a trend (P=0.07)
for a greater decrease in obese women (fig 3). Because
of decreases in insulin sensitivity over time fat oxidation
increased 220% in both lean and obese women
(P=0.003).
There was decreased suppression of lipolysis during
insulin infusion (hyperinsulinemic-euglycemic clamp),
but no significant difference between groups (P=0.30).
Basal free fatty acids decreased 16% over time (P=0.02)
but free fatty acids increased by 62% during insulin
infusion with the clamp over the course of pregnancy
responses to obesity is that most information comes from
studying late gestation placentas.
In contrast to increased inflammatory markers, concentrations
of placenta and plasma estradiol and progesterone
are lower in obese than in lean women.47 During
pregnancy, estradiol and progesterone are synthesized
in placental mitochondria from cholesterol precursors.
Although there are no significant differences in circulating
or placental cholesterol concentrations, mitochondrial
cholesterol concentrations are 40% lower in the
placentas of obese women, and this is related to decreases
in the mitochondrial cholesterol translocator protein.47
The clinical significance of the decrease in placental
steroid production is unknown but may be related to the
adverse perinatal outcomes seen in obese women.
In summary, in early pregnancy the human placenta is
responsive to the high concentrations of maternal insulin
found in obese women. This results in altered gene
expression in relation to mitochondrial steroid hormone
production and energy metabolism. Furthermore, pla-
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Fig 2 | Longitudinal changes in body composition in lean and
obese women before pregnancy through to late gestation.
(A) Changes in lean body mass (kg; mean and standard
deviation) in lean (n=5) and obese (n=6) women:
prepregnancy, early pregnancy (12-14 weeks), and late
pregnancy (34-36 weeks). Change over time, P=0.0001 and
between groups, P=0.34. (B) Longitudinal changes over time
(kg; mean and standard deviation) of fat mass in lean (n=5) and
obese (n=6) women: prepregnancy, early pregnancy (12-14
weeks) and late pregnancy (34-36 weeks). Change over time,
P=0.0001 and between groups, P=0.0253
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Fig 3 | Longitudinal changes in insulin sensitivity in lean and
obese women before pregnancy through to late gestation.
Longitudinal changes over time in insulin sensitivity (mean
and standard deviation) as estimated by the hyperinsulinemiceuglycemic
clamp (mg/kg.ffm/min) in lean (n=5) and obese
(n=6) women: prepregnancy, early pregnancy (12-14 weeks)
and late pregnancy (34-36 weeks). Change over time,
P=0.0001 and between groups, P=0.0753
BMJ: first published as 10.1136/bmj.j1 on 8 February 2017. Downloaded from http://www.bmj.com/ on 13 February 2021 at Medical Sciences Library Texas A & M University. Protected by copyright.
STATE OF THE ART REVIEW
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obese women with average for gestational age neonates.59
The decreased fetal-maternal amino acid gradients seen
in some obese women may be related to altered placental
amino acid transporter activity41 and decreased placental
SNAT activity.60
In summary, significant decreases in insulin sensitivity
(increased insulin resistance) occur during pregnancy,
with obese women showing greater decreases in insulin
sensitivity. In addition to affecting glucose metabolism,
decreases in insulin sensitivity

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