Abstract
Prevalence rates of maternal obesity are increasing. One of the leading causes is excessive gestational weight gain (GWG) during pregnancy as defined by the 2009 American Institute of Medicine guidelines. Excessive GWG can cause adverse effects in both the mother and offspring including; increased rates of caesarean section, post-partum infection and gestational diabetes mellitus in the mother and higher risk of cardiovascular disease, diabetes and obesity in the offspring.
The aim of this report was to review the evidence regarding the impact of excess maternal GWG on development of obesity in subsequent offspring during childhood.
Seven original research papers were studied encompassing the obesity effects on children from 2-7years of age with additional evidence including studies of children up to 11years. The main findings were summarised and critically reviewed using the supporting evidence.
The evidence found a significant relationship between excessive gestational weight gain and childhood obesity, generating a mean increased risk of 38.86%. Differences in methodology between the studies, such as guidelines and measurements used, may decrease the reliability and impact of the results. Controversies existed within the research findings, regarding mechanisms linking GWG and childhood obesity, the shape of the relationship and interactions with cofounding variables. Further research into such controversies is required before significant conclusions can be made.
Word count: 212
Key words: Maternal obesity, gestational weight gain, childhood obesity, adverse childhood effects, foetal programming.
Running Head: Gestational weight gain and childhood obesity.
1. Introduction to maternal obesity, Gestational weight gain and adverse outcomes.
Maternal obesity is defined as having a Body Mass Index (BMI) ≥30kg/m² at any point during pregnancy (CMACE, 2010). Prevalence rates of maternal obesity are increasing; Heslehurst et al (2010) conducted a national maternal obesity study of England between 1989 and 2007 and found that rates doubled from 8% to 16% (equivalent of 45,064-92,501 women) over the study duration. Similarly, the CMACE Maternal Obesity Report (2010) states that approximately 7.19% of women in the UK have a BMI in obese class 2 or above (BMI ≥35kg/m²).
Maternal obesity can result in serious adverse effects on the mother and offspring (Avci et al, 2015), obese women have a higher risk of requiring a caesarean section, post-partum infection and prevalence of gestational diabetes mellitus (Santangeli et al, 2015). Long-term risks have also been recognised including; cardiovascular diseases, diabetes and obesity (Aviram et al, 2011). Obesity in childhood can cause comorbidities such as; metabolic syndrome, pulmonary and gastrointestinal morbidities, psychosocial issues and early puberty onset (Yanovski et al, 2015).
Gestational weight gain (GWG) is a biological process which functions to support development of the foetus during a pregnancy by managing maternal and foetal metabolism and physiology (IOM, 2009). Some weight gain is essential to avoid adverse perinatal outcomes including; pre-eclampsia, macrosomia and low birth weight (Langford et al, 2011), however if excessive, it can contribute to adverse effects associated with maternal obesity. Excessive GWG is that which is above the guidelines for the individuals’ pre-pregnancy BMI category (table 1). The American Institute of Medicine (IOM) guidelines are commonly used (table 1) as there are no UK guidelines at present (MoDP, 2014). This review will focus on the effect of GWG on offspring body weight during childhood up to the age of 11 years.
The aim of this paper is to review research evidence on the impact of maternal obesity (specifically gestational weight gain) on development of obesity in the offspring during childhood (up to 11years).
Word count: 333
2. Effect of excess GWG on offspring’s future health.
Research investigating the link between GWG and development of childhood obesity has found strong relationships, suggesting that gaining excessive GWG (according to IOM guidelines, table 1) significantly increases the risk of the offspring developing obesity during childhood. Table 2 provides a summary of evidence in children between 2-7years of age. The mean increased risk for childhood obesity following excessive GWG was 38.86%. Additionally, results from a meta-analysis by Tie et al (2014) found a mean 33% increased risk in childhood obesity for mothers who gained excessive gestational weight, even after adjusting for pre-pregnancy BMI, demographics and child age. Similar results were gathered in a meta-analysis by Mamun et al (2014) who found a mean increased childhood obesity risk of 40% following excess maternal GWG. Supporting evidence encompasses research for offspring up to 11years.
3. Mechanisms influencing excess GWG on development of obesity in offspring.
Several mechanisms have been proposed to explain the link between excessive GWG and childhood obesity. One of the main recurring mechanisms is; developmental or foetal programming. The foetal origins hypothesis (Barker, 1995) was the first theory to suggest that unfavourable nutritional circumstances within the intrauterine environment could contribute to the development of obesity, cardiovascular disease and type 2 diabetes in childhood and even into adulthood (Desai et al, 2013).
This mechanism is supported by several authors (Sridhar et al (2014), Wrotniak et al (2008) and Gluckman & Hanson (2008)) where they suggest that pre-disposition to obesity can begin in the intrauterine environment, through epigenetic pathways. It is postulated that intrauterine exposure to excessive GWG (over nutrition) is thought to permanently alter infant metabolism, through alteration of the genome (insulin sensitivity in particular), leading to increased risk of excessive weight gain in childhood (Sridhar et al, 2014) This is a similar process to that seen as a result of gestational smoking and diabetes mellitus (Oken et al, 2007).
Gluckman and Hanson (2008) and also Wrotniak et al (2008), suggested that consistent over-exposure of the foetus to high glucose levels could lead to hyperinsulinemia. This may not only increase the volume of adipose cells laid down in utero; but can also lead to insulin resistance, which increases obesity risk in early childhood and type 2 diabetes in later life.
However, another mechanism is the hormonal or neural pathway (Sen et al, 2012) which suggests that maternal obesity disrupts development in a section of the hypothalamus involved in energy regulation; possibly by altering levels of leptin which is also involved in regulation of energy, satiety and appetite.
Although this evidence suggests possible explanations to the mechanisms, it fails to show a clear structure for the pathways. Sen et al (2012) explains that the pathways which link maternal over nutrition and offspring obesity are not necessarily isolated and can occur simultaneously to contribute to childhood adiposity.
4. Effect of gestation of excessive GWG on development of Obesity in childhood.
The stage of gestation during pregnancy where excessive weight is gained is believed to be influential in the development of offspring obesity. Evidence suggests (Anderson et al (2011) and Bayer et al (2014)) that weight gain the 1st and 2nd trimesters is significantly more likely than weight gain in the 3rd trimester to contribute to offspring obesity. Similarly, Karachaliou et al (2015) found that GWG in the 1st trimester was most influential towards childhood obesity. That is not to say that GWG in the later stages of pregnancy does not have adverse effects, Karachaliou found that GWG in the 3rd trimester posed a greater risk for high infant birth weight and high levels of blood cord leptin.
Therefore controversy exists as to the exact gestation when excessive GWG influences offspring obesity; it is possible that the impact of excessive GWG should not be assessed over the gestation as a whole; which has been the case in much of the research to date.
5. Evidential variation in the shape of the relationship between GWG and childhood obesity.
Evidence has proven that excessive GWG causes an increased risk of childhood obesity, but controversy has arisen regarding the link between childhood obesity risk and inadequate GWG, this can be referred to as the shape of the relationship. While some of the literature reports finding a linear relationship; where low GWG decreases risk of childhood overweight (Guo et al 2015 & Wrotniak et al, 2008), some report a U/J-shaped relationship whereby both inadequate and excessive GWG significantly increase childhood obesity risk (Sridhar et al, 2014). Other research suggests no relationship between inadequate GWG and childhood obesity risk (Ensenauer et al, 2013 & Henriksson et al, 2014).
The main mechanism suggested to account for a U/J-shaped relationship between GWG and subsequent obesity is derived from Gluckman and Hanson’s 2008 review (supported by Berends et al, 2013) and is named the “mismatch pathway”. It suggests that undernutrition in the intrauterine environment can alter gene expression in such a way that the foetus has adapted itself to an energy-deficient environment, in order to increase its chance of survival. When the child is then born and exposed to an obesogenic environment to which it is not adapted, it is at higher risk of metabolic compromise and obesity as it grows (Parlee & MacDougald, 2014).
6. Association between pre-pregnancy BMI, GWG and childhood obesity.
One of the main arguments within the literature is whether or not there is a significant interaction between pre-pregnancy BMI, excessive GWG and subsequent childhood obesity; or if they independently contribute to childhood obesity risk. In other words, does pre-pregnancy BMI mediate or exaggerate the effect of excess GWG on childhood obesity, or is there no link. The likelihood of a significant interaction is low however; most studies adjusted for pre-pregnancy BMI during significance calculations. Also, literature suggesting an interaction has been inconsistent; Sridhar et al (2014) and Diesel et al (2015) found that excessive GWG may pose a higher obesity risk on the infants of normal weight mothers, yet Guo et al (2015) found the highest risk among children of overweight /obese mothers. In further contrast, Wrotniak et al 2008 found a greater childhood obesity risk when mothers were underweight pre-pregnancy and Oken et al (2007) found no interaction. An extended literature search should be carried out to be able to draw an explanatory conclusion for this variation in results.
7. Comparison across research with varying methodologies.
It is questionable whether or not it is appropriate to compare studies across different ages. Although a small age range, early and young childhood is a period of rapid growth and change with a multiplicity of influences (Cebeci & Guven, 2015). Wrotniak et al (2008) suggested that as age increases throughout childhood the link between GWG and obesity decreases. This is understandable; the child may still be obese, but as a result of other influences. Yanovski (2015) in his review of paediatric obesity demonstrates how the scope of a child’s influences get larger and expand from caregivers and close family, to school, peers and the community.
Other differences across the literature include the statistical and reference values used; for example Wrotniak et al (2008) and Oken et al (2007) based results on IOM 1990 GWG guidelines which are slightly different to the 2009 ones used in more recent studies however these were the values available at this time and are only different in that they have a specific obese weight gain range rather than a minimum amount. That said, the difference in guidelines should not be an issue as stated by Nehring et al (2012) who faced a similar problem in their review of GWG and childhood obesity.
Similarly, differences in definition of GWG were found (table 2); Mourtakos et al (2015) and Guo et al (2015) defined GWG as the difference between first and last medical weigh-ins however the other studies calculated GWG based on self-reported pre-pregnancy BMI’s. Using self-reported data increases bias risk and decreases reliability in the results as under or over-reporting may have occurred.
There is a large scope of factors that can influence childhood obesity including; maternal BMI, physical activity, child energy intake and eating patterns and environment (family, school and neighbourhood) for example (Proctor, 2007). It can be seen in table 2 that all studies attempted to adjust for confounding factors when interpreting their results. However whenever these adjusted factors are different between studies, comparison between studies may not be appropriate. For example, Diesel et al (2015) and Ensenaeur et al (2013) adjusted their results for the effects of breastfed children yet none of the other studies did, if breastfeeding were to have an effect, then comparison of these studies with the others would not be valid.
The multiplicity of confounding factors faced owes to the fact that the majority of studies in this area are observational. It is reasonable that few intervention studies are available as ethics and practicality would limit the extent of intervention.
9. Conclusion
Maternal obesity rates are increasing and subsequent effects are becoming apparent, not only in the mother but also in her offspring. From the evidence reviewed it can be concluded that there is a significant relationship between excessive gestational weight gain (according to Institute of Medicine guidelines) and the risk of offspring developing obesity between the ages of 2-11, even after adjustment for relevant confounding factors (mean increased risk of 36.86%).
Areas for further research include; mechanisms linking gestational weight gain to childhood obesity, the shape of the association (U/J-shaped or linear) and the interaction between pre-pregnancy Body Mass Index, gestational weight gain and their link to development of childhood obesity.
Total word count: 1931
Reference List
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Appendix 1
Table 1: Body Mass index (BMI) and IOM (2009) recommended Gestational Weight Gain guidelines.
BMI Category (Range in kg/m²)* Gestational Weight Gain Range (lbs)** Gestational Weight Gain Range (kg)***
Underweight (<18.5) 28-40 12.7-18.2
Normal Weight (18.5-24.9) 25-35 11.4-16
Overweight (25-29.9) 15-25 6.8-11.4
Obese – all classes (≥30) 11-20 5-9
*sourced from WHO (2006) **sourced from Institute of Medicine (2009) ***assumes 2.2lbs=1kg.
Table 2: Comparison of research regarding GWG and its impact on childhood obesity.
Study of the relationship between GWG % risk of childhood obesity Sample size (n=mother-child pairs) Child age at follow-up (years) Confounding factors accounted for: Definition of GWG
Sridhar et al (2014) 46 4145 2-5 Maternal age, education level, parity, ethnicity, pre-pregnancy BMI, physical activity level, child gender and birthweight. Difference between last pregnancy weight and self-reported pre-pregnancy weight.
Wrotniak et al (2008) 48 10,226 7 Pre-pregnancy BMI, maternal age, ethnicity, smoking status, parity, child gender and birthweight Difference between last pregnancy weight and self-reported pre-pregnancy weight.
Guo et al (2015) 21 100,612 3-6 Maternal age, pre-pregnancy BMI, education, occupation, gravidity, parity, gestation, child gender and birthweight. Difference between weight at delivery and initial medical examination.
Ensenauer et al (2013) 57 6837 5.8 Maternal age, pre-pregnancy BMI, parity, socioeconomic status, child gender, birthweight, BMI, activity level, sedentary level, breastfed status and waist circumference. Difference between last pregnancy weight and self-reported pre-pregnancy weight.
Oken et al (2007) 35 1044 3 Maternal age, pre-pregnancy BMI, ethnicity, parity, income, paternal BMI, pre-natal glucose tolerance, child BMI, gender, birthweight and gestation. Difference between last pregnancy weight and self-reported pre-pregnancy weight.
Diesel et al (2015) 20 609 3 Maternal age, pre-pregnancy BMI, smoking status, smoking pattern, alcohol use, marijuana use, education, occupation, income, marital status, gestation, child BMI, gender and breastfed status. Difference between last pregnancy weight and self-reported pre-pregnancy weight.
Mourtakos et al (2015) 45 5125 8 Pre-pregnancy BMI, smoking status, alcohol consumption, exercise level, child BMI, gender, birth weight. Difference in weight between first and last GP visits.