Series (year) [reference]
Design
Sample/setting
Maternal obesity measure
Cardiometabolic outcome
Age at follow-up
Key findings
Blood pressure
Filler et al. (2008) [31]
Cohort
Children’s Hospital, London Health Science Centre, UK
N = 1,915 children
Pre-pregnancy BMI reported retrospectively by mother at 24–28 weeks GA
Systolic blood pressure [SBP] and diastolic blood pressure [DBP]
Mean age = 8.3 ± 5.2 years
BMI z-score correlated significantly with SBP (Spearman r = 0.214, p < 0.0001), and DBP z-scores (Spearman r = 0.143, p < 0.0001)
Lawlor et al. (2004) [32]
Cohort
Mater-University study of pregnancy and its outcomes (MUSP)
N = 3,864
Maternal pre-pregnancy BMI
Systolic blood pressure [SBP]
5
For every standard deviation unit increase in maternal pre-pregnancy BMI, there was a 0.38 increase in SBP, respectively (p < 0.05), after adjustment for potential confounders
Wen et al. (2011) [33]
Cohort
Collaborative Perinatal Project
N = 30, 461
Maternal pre-pregnancy BMI
Systolic blood pressure [SBP]
7
Compared to normal weight, pre-pregnancy overweight obesity was associated with a higher offspring SBP (0.89 mmHg 95 % CI: 0.52, 1.26)
Laor et al. (1997) [34]
Cohort
Jerusalem
N = 10,883
Maternal pre-pregnancy BMI
Systolic blood pressure [SBP] and diastolic blood pressure [DBP] from military draft records
17
Women: Pearson correlation 0.053 and 0.049 for SBP and DBP, respectively
Men: Pearson correlation 0.053 and 0.060 for SBP and DBP, respectively
Hochner et al. (2012) [35]
Cohort
Jerusalem Perinatal Study [JPS]
N = 1,400
Maternal pre-pregnancy BMI
Systolic blood pressure [SBP] and diastolic blood pressure [DBP]
32
For every unit increase in maternal pre-pregnancy BMI, there was a 0.441 and a 0.287 increase in SBP and DBP, respectively (p < 0.05)
Fraser et al. (2010) [36]
Cohort
Avon Longitudinal Study of Parents and Children [ALSPAC]
N = 3,457
Maternal pre-pregnancy weight
Systolic blood pressure [SBP] and diastolic blood pressure [DBP]
9
For every unit increase in maternal pre-pregnancy weight, there was a 0.108 increase in SBP (95 % CI: 0.087, 0.130)
For every unit increase in maternal pre-pregnancy weight, there was a 0.028 increase in SBP (95 % CI: 0.013, 0.043)
Metabolic markers
Mingrone et al. (2008) [37]
Case control
N = 67
Cases = 52
Offspring of mothers with BMI ≥30 kg/m2
Control = 15
Offspring of mothers with normal weight, BMI <25 kg/m2
Maternal pre-pregnancy BMI
Insulin sensitivity calculated from OGTT
23.8 ± 4.5 years
Cases were more insulin resistant than controls
Women: (398.58 ± 79.32 vs. 513.81 ± 70.70 ml−1 · min−1, p < 0.0001; Men: 416.42 _ 76.17 vs. 484.242 ±45.76 ml−1 · min−1, p < 0.05)
Insulin secretion after OGTT was higher in cases than control
Men: (63.94 ± 21.20 vs. 35.71 ± 10.02 nmol · m−2, p < 0.01) but did not differ significantly in women
Hochner et al. (2012) [35]
Cohort
Jerusalem Perinatal Study [JPS]
N = 1,400
Maternal pre-pregnancy BMI
Insulin
Glucose
LDL
HDL
Triglycerides
32
For every unit increase in maternal pre-pregnancy BMI, there was a 0.008 increase in insulin (p = 0.007)
For every unit increase in maternal pre-pregnancy BMI there was a 0.001 decrease in glucose (p = 0.875)
For every unit increase in maternal pre-pregnancy BMI, there was a 0.010 decrease in HDL (p = 0.033)
For every unit increase in maternal pre-pregnancy BMI, there was a 0.012 (p = 0.240) and a 0.007 (p = 0.020) increase in LDL and triglycerides, respectively
Fraser et al. (2010) [36]
Cohort
Avon Longitudinal Study of Parents and Children [ALSPAC]
N = 3,457
Maternal pre-pregnancy weight
Lipids: HDL, triglycerides
9
For every unit increase in maternal pre-pregnancy weight, there was a 0.002 decrease in HDL (95 % CI: −0.003, −0.001)
For every unit increase in maternal pre-pregnancy weight, there was a 1.002 increase in triglycerides (95 % CI: 1.000, 1.003)
There have only been a few studies to examine the relationship between maternal obesity and blood pressure [31–35]. Most of these have examined blood pressure during childhood only [31–33], and just one study has examined offspring blood pressure during adolescence [34] and in adulthood, respectively [35]. These studies consistently report a significantly positive association between maternal obesity and blood pressure as shown in Table 11.1. To our knowledge, to date, only two studies have examined the association between maternal obesity and metabolic markers such as insulin and glucose in offspring beyond 1 year. Mingrone et al. [37] compared insulin sensitivity, insulin secretion, and body composition in offspring of obese mothers with those born to mothers with normal weight. They found that offspring of obese mothers were significantly more insulin resistant (410 ± 91 vs. 500 ± 60 ml−1 · min−1) and had higher prevalence of hyperinsulinemia than offspring of normal weight mothers, but found no difference in β-cell glucose sensitivity impairment. Similarly, in the Jewish Perinatal Family Follow-Up Study birth cohort, Hochner and colleagues investigated the association between maternal obesity and cardiometabolic risk factors in offspring at age 32 [35]. In this study, maternal obesity was independently associated with insulin, triglycerides levels, and lower HDL as shown in Table 11.1. These findings concur with the findings of Catalano et al. who reported that at birth, offspring of obese mothers had higher insulin resistance, leptin, and IL-6, suggesting that maternal obesity results in a high cardiometabolic risk phenotype, with increased cardiometabolic risk beginning at birth [38]. One study [11] examined the association between maternal obesity and metabolic syndrome in offspring. Boney et al. [11] reported an independent effect of maternal obesity on risk of metabolic syndrome in a study of 179 children at ages 6–11 years.
Asthma
Previous studies have found that obesity and asthma occur concurrently in both children and adults. However, the causal direction and mechanisms are not understood [39]. Overweight is associated with increased levels of proinflammatory cytokines. As such, offspring of obese mothers are exposed to increased levels of proinflammatory cytokines during fetal development which may affect the immunological and pulmonary development and result in asthma symptoms after birth. There is a very small body of literature on the association between maternal obesity and asthma and asthma-related symptoms [40–46]. All of these studies consistently show an increased risk of asthma [41, 43–46] or wheezing [40, 42] as shown in Table 11.2 among children between 6 months and 16 years for offspring of mothers who are obese compared to offspring of nonobese mothers. One study even demonstrated a dose response relationship between the degree of maternal overweight status during pregnancy and increased risk of asthma in the offspring [43].
Table 11.2
Obesity during pregnancy and asthma in the offspring
|
Series (year) [reference] |
Design |
Sample/setting |
Maternal obesity measure |
Asthma measure |
Age at follow-up |
Findings |
|---|---|---|---|---|---|---|
|
Reichman et al. (2008) [45] |
Birth cohort study |
Fragile Families and Child Wellbeing study, an ongoing longitudinal birth cohort study 1998–2000 75 hospitals in 20 US cities
N = 1,971 |
Pre-pregnancy weight and height abstracted from medical record |
Maternal interview self-report |
3 years |
Obese mothers had 52 % higher odds than nonobese mothers of having a child diagnosed with asthma (OR = 1.52; 95 % CI: 1.18, 1.93) in the univariate and a 34 % higher odds (OR = 1.34; 95 % CI: 1.03, 1.76) after adjustment for covariates (sociodemographic, medical obstetric, and behavioral factors) |
|
Harpsoe et al. (2013) [41] |
Danish birth cohort study |
N = 38,874 mother-child pairs from the Danish National Birth Cohort [DNBC] (enrollment 1996–2002) |
Self-reported weight and height measures from baseline interview and self-reported gestational weight gain |
Self-reported doctor-diagnosed asthma |
7 years |
Compared with children of normal weight mothers, children of mothers with high BMI had significantly increased odds of doctor-diagnosed asthma ever (p < 0.0001), children of obese mothers (adjusted OR, 1.54; 95 % CI: 1.34, 1.76) or very obese (adjusted OR, 1.52; 95 % CI: 1.21, 1.91)
The odds of doctor-diagnosed asthma ever increased significantly with increasing GWG (p = 0.01) with the highest odds among mothers gaining ≥25 kg during pregnancy compared with mothers gaining 10–15 kg (adjusted OR, 1.17; 95 % CI: 1.02, 1.33) |
|
Patel et al. (2012) [44] |
Prospective cohort study |
Northern Finland birth cohort
July 1985–June 1986
N = 6,945 |
Pre-pregnancy and height were abstracted from medical record and BMI calculated |
Self-reported asthma symptoms |
15–16 years |
High maternal pre-pregnancy weight was significantly associated with ever asthma in adolescents (OR = 1.28, 95 % CI: 1.06, 1.54 and for current asthma; OR = 1.30, 95 % CI: 1.01, 1.67 for current asthma)
Higher maternal pre-pregnancy weight in the top tertile was significantly associated with an increase in the risk of ever wheeze and current wheeze (OR = 1.22, 95 % CI: 1.01, 1.47 and OR = 1.52, 95 % CI: 1.19, 1.95), respectively |
|
Lowe et al. (2011) [43] |
Retrospective cohort study |
Sweden. All children born in Stockholm County, Sweden between 1998 and 2009
N = 129,329 |
BMI calculated from initial antenatal visit (8–10 weeks of gestation)
BMI ≥ 30 |
Asthma in offspring |
Higher maternal BMI was consistently associated with an increased risk of asthma in the child both in terms of medicine use and hospitalization
Association was linear at all ages. At age 6–8 years, the effect of maternal BMI was somewhat stronger in girls (OR = 1.04, 95 % CI: 1.02, 1.05) per unit increase in BMI) than in boys (OR = 1.01, 95 % CI: 1.00, 1.03); p for interaction = 0.01) and was also weaker in fourth and subsequent children (p for interaction = .03) | |
|
Haberg et al. (2009) [40] |
Cohort study |
Norwegian mother and child cohort study (MoBa)
N = 33, 192 |
Maternal BMI calculated from self-reported pre-pregnancy weight and height obtained via questionnaire |
Lower respiratory tract infections [LRTIs], hospitalization for LRTIs and wheeze reported at 6 and 18 months after birth obtained via self-report |
6, 18 months |
The risk of wheeze increased linearly with maternal
BMI in pregnancy and was 3.3 % higher (95 % CI: 1.2, 5.3) for children with mothers who were obese during pregnancy than for children of mothers with normal BMI |
|
Kumar et al. (2010) [42] |
Cohort |
N = 1,191
Boston Birth Cohort (1998-present) followed to a mean age of 3.0 ± 2.4 years |
Self-reported pre-pregnancy weight and height |
Recurrent wheezing (4 or more episodes of medically attended wheezing illness in the subject’s life time using electronic medical record abstraction) |
~3 years |
Children of obese mothers (BMI ≥ 30) had an increased risk of recurrent wheezing OR = 3.51, 95 % CI: 1.68, 7.32 |
|
Scholtens et al. (2010) [46] |
Cohort |
N = 3,963 participants in the prevention and incidence of asthma and mite allergy study |
Self-reported pre-pregnancy weight and height |
Self-reported wheeze, dyspnea, and use of prescription inhaled corticosteroids |
8 years |
Among children predisposed to asthma (n = 1,058, i.e., having at least one parent with asthma), pre-pregnancy overweight was associated with increased risk of asthma at 8 years (OR = 1.52, 95 % CI: 1.05, 2.18) |
Neurodevelopmental Outcomes
The cardiovascular and endocrine systems may not be the only systems altered by maternal obesity during pregnancy. In fact, a systematic review suggests that infants born to obese mothers are at increased risk of central nervous system (CNS) developmental problems [47]. There is substantial evidence from animal models which suggests that maternal obesity increases the risk of the development of neurological and psychological dysfunction. Results from extant human studies provide additional support that maternal obesity may be linked to mental health disorders in children as summarized in Table 11.3. In a recent systematic review [58] of 12 studies reviewed, five provided clear support for an association between maternal obesity and neurodevelopmental problems including childhood IQ [53], attention-deficit/hyperactivity disorder [ADHD] [55], schizophrenia [49, 51], and eating disorders [59].
Table 11.3
Obesity during pregnancy and long-term neurodevelopment outcomes in offspring
|
Series (year) [reference] |
Design |
Sample/setting |
Maternal obesity measure |
Neurodevelopmental outcome |
Age at follow-up |
Key findings |
|---|---|---|---|---|---|---|
|
Jones et al. (1998) [48] |
Cohort study |
Finland (N = 10,578) |
Pre-pregnancy BMI reported retrospectively by mother at 24–28 weeks GA |
Schizophrenia (psychiatrist diagnosed using DSM III R) |
28 years |
Odds ratio [OR] = 2.1, 95 % Confidence Interval [CI]: 0.9, 4.6 for children of mothers with BMI > 29 kg/m2 compared with children of mothers with BMI 19.1–29.0 kg/m2 |
|
Schaefer et al. (2000) [49] |
Cohort study |
Child Health Development Study [CHDS], USA
Births between 1959 and 1967
63 cases of schizophrenia and 6,570 unaffected offspring |
BMI measured at study enrolment by healthcare personnel |
Schizophrenia and spectrum disorders diagnosed using the DIGS |
30–38 years |
Relative Risk [RR] = 2.9, 95 % CI: 1.3, 6.6 for children of mothers with BMI > 30 kg/m2 compared with BMI 20.0–26.9 kg/m2 |
|
Wahlbeck et al. (2001) [50] |
Cohort study |
Prospective birth cohort, Finland
Births between 1924 and 1933
N = 7,086 |
Late pregnancy BMI from birth records |
Schizophrenia diagnosis obtained from Hospital Discharge Register |
Offspring had a small increased odds of schizophrenia for each unit decrease in maternal late pregnancy BMI (OR = 1.09, 95 % CI 1.02–1.17)
Compared to offspring of mothers with a late pregnancy BMI >30, those with mothers with late pregnancy BMI <30 had around a threefold increased odds of schizophrenia | |
|
Kawai et al. (2004) [51] |
Case–control study |
Japan cases: N = 52, controls: N = 6,570 born on or after 1966 |
BMI measured at first and last antenatal care visits by clinic personnel |
Schizophrenia (psychiatrist diagnosed using DSM IV) |
19 |
For every 1 unit increase in early pregnancy BMI, odds of schizophrenia increased 24 % (OR = 1.24, 95 % CI 1.02–1.50)
For every one unit increase in late pregnancy BMI, odds of schizophrenia increased 19 % (OR = 1.19, 95 % CI 1.00, 1.41) |
|
Krakowiak et al. (2012) [52] |
Case–control study |
California, USA. Data of children enrolled in the CHARGE (Childhood Autism Risks from Genetics and the Environment) study
N = 1,004; ASD(517), DD(172), Control(315) |
BMI ≥ 30, with onset before pregnancy |
Autism spectrum disorder [ASD], developmental delays [DD] |
The risk of having a child with ASD or DD, relative to typical development [TD] was significantly increased among obese women (ASD, OR: 1.67 [95 % CI: 1.10–2.56]; DD, OR: 2.08 [95 % CI: 1.20–3.61]); >20 % of case mothers were obese compared with 14.3 % of controls. The prevalence of any MC was higher in the ASD (28.6 %) and DD (34.9 %) groups compared with controls (19.4 %), with respective adjusted ORs of 1.61 (95 % CI: 1.10–2.37) and 2.35 (95 % CI: 1.43–3.88).
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