Maternal obesity

Tahir A. Mahmood and Rohan Chodankar

Epidemiology

Obesity presents one of the greatest cross-disciplinary challenges to practicing clinicians worldwide, and in many ways defines the changing face of modern obstetrics and gynecology. It is a global pandemic that affects both high- and low-middle-income countries and poses a serious public health problem (1). This is reflected in a rising incidence in the pattern of all forms of hyperglycemia in pregnancy (HIP), diabetes during pregnancy, and gestational diabetes.

Obesity has been recognized by the World Health Organization (WHO) as a noncommunicable disease. Of late, more attention has been paid to the long-term consequences of HIP in the offspring, with a particular focus on its long-term health consequences as an adult and on intergenerational and transgenerational effects (1,2).

The toll of obesity on healthcare systems is significant and accounts for 2% and 7% of all healthcare spending in the developed countries. This does not include the cost of treating associated disease, which may increase the healthcare cost by up to 20% according to some estimates (3).

Three UK studies have shown that the incidence of maternal obesity increased from 3.2% to 8.9% between 1990 and 1999 in Cardiff, from 9.4% to 18.9% between 1990 and 2002–2004 in Glasgow, and from 9.9% to 16% between 1990 and 2004 in Middlesbrough (4–6). There is an absence of national statistics for maternal obesity in the United Kingdom. Within European Union (EU) countries, the prevalence of maternal obesity varies from 7% to 25%, and has been shown to increase in some regions from 10.2% in 2009 to 11.4% in 2014 (7).

Similar concerns have been expressed in the United States. The increasing incidence of obesity among females of reproductive age is of particular concern, with cross-sectional data now estimating an overall prevalence of 32.4% in the United States. The prevalence of grade I (body mass index [BMI] 30–34.9 kg/m2) and grade II (BMI 35–39.9 kg/m2) obesity has doubled since 1979 and that of grade III (BMI >40 kg/m2) obesity increased threefold over the same period (2009). Data from the Pregnancy Risk Assessment Monitoring System (PRAMS database) show a pre-pregnancy incidence of obesity in the United States of 20%. This represents an overall increase of 70% over a 10-year period (8). Several other studies support the rising trend of obesity in the United States with an impact on women of childbearing age (9–11).

Genetics

The first evidence that genetics is important in common nonsyndromic obesity came from a study published nearly 30 years ago that reported that the observed familial aggregation for obesity was due to genetic factors rather than environmental influences (12). Another study also observed that adopted children had body sizes more similar to those of their biological parents rather than their adopted parents (13).

Studies from twins have yielded interesting observations. It appears that fat mass is genetically influenced among individuals who are more genetically similar, such as in the case of monozygotic twins versus dizygotic twins (14). Even for twins reared apart, the estimated heritability was 65%–75% for BMI (15).

The relative contribution of energy intake and expenditure in the development of obesity may also have a genetic basis. Bouchard et al. reported that overfed pairs of twins and within twin pairs, weight-gain correlation was high (>70%). Interestingly, after the study, most subjects spontaneously returned to their original food intake behavior and lost weight, and this reduction was also found to be genetically driven (16). This phenomenon was also confirmed in Czech twins in another study (17).

A role for the monogenic origins of obesity was first proposed with studies in murine models, followed by a similar discovery in humans. Experiments with a series of mouse obesity genes, including those that encode leptin, the leptin receptor (LEPR), carboxypeptidase E (responsible for processing prohormone intermediates, such as proinsulin, and the orexigenic protein agouti), allowed for significant improvements in knowledge (18–21). Targeted genetic manipulation has also established the vital regulatory role of molecules such as the melanocortin 4 receptor (MC4R), which is vital in the melanocortin pathway, and the orexigenic protein AGRP (22,23). Monogenic recessive forms of human obesity caused by mutations in the genes that encode leptin, LEPR, prohormone convertase 1 (an endopeptidase that is involved in processing prohormones, including insulin and POMC), and POMC, all of which result in a phenotype of excessive energy intake relative to energy expenditure were subsequently discovered (24–27). More frequent forms of obesity are caused by mutations in the gene that encodes MC4R. MC4R deficiency (autosomal-dominant) represents the most common monogenic obesity disorder that has been identified so far (28).

Furthermore, the results of longitudinal behavior genetic studies suggest that there are age-specific genetic effects on BMI. The “Human Obesity Gene Map” has been available since 1994, and the latest update had been in 2005 (29). This comprehensive compendium summarizes the evidence from the four classes of human studies:

1.Obesity due to a single gene in digenic mutation.

2.Obesity associated with Mendelian disorders such as Prader–Willi syndrome or Bardot-Biedl syndrome.

3.Associated studies that test whether candidate genes are associated with obesity phenotypes among samples of unrelated participants.

4.Linkage studies that test for causal association between genomic regions and obesity phenotypes in a cohort of families.

It is beyond the scope of this chapter to discuss the syndromic origins of obesity. Louwen et al. have reported that adipose-derived mesenchymal stem cells (ASCs) in obesity are defective in various functionalities and properties, including differentiation, angiogenesis, motility, multipotent state, metabolism, and immunomodulation. Inflammatory milieu, hypoxia, and abnormal metabolites in obese tissue are crucial for impairing the functions of ASCs (30).

Psychological basis of obesity

The relationship between obesity and psychological health has long been controversial and remains poorly understood. A summary of potential risk factors is listed in Table 8.1.

Obesity studies have identified a positive correlation between obesity and poor body image, low self-concept, and negative attributions of life events (31). Psychological comorbidities such as depression, anxiety, and altered personality traits are also known to be associated with obesity (32). Subsequent studies aimed to identify behavioral risk factors associated with psychological problems in obese individuals. Positive correlations were found with dieting (cognitive restraint eating), binge eating, and weight cycling (the repeated loss and regain of weight through attempts at dietary behavior modification) (33,34).

Three mains groups of psychological obesity have been described:

•Schizoid obese patients are said to display a lack of autonomy, with difficulty in establishing boundaries between self and nonself, and they experience surreal feelings of being governed by external forces. They invariably fail most weight-loss intervention programs.

•Egodystonic obese patients often display reactive depression and anxiety, and they have a continuous need for comfort eating, with repeated dietary attempts at weight loss and a high index of cognitive restraint eating.

•Egosyntonic obese patients develop obesity for a variety of reasons that might be personal, familial, hereditary, or even cultural. Despite their obesity, these people live without psychological problems. They are often characterized by being extrovert, talented people, with a good sense of reality and body image, but with a total inability to resist social eating cues (33).

Newer research studies are now investigating the multifactorial origin of obesity by integrating genetic, physiological, and psychological components in longitudinal studies in order to establish causality and determine tailored treatments in keeping with the concept of personalized precision medicine.

Measurement of obesity and risk of morbidity

It is widely accepted that being overweight is a major risk factor for a wide range of chronic diseases, including cardiovascular disease (CVD), type II diabetes, and certain site-specific cancers, including colorectal and breast cancers (35,36). Although BMI has traditionally been the chosen method by which to measure the body, alternative measures such as waist circumference (WC), waist-to-hip ratio (WHR), and waist-to-height ratio (WHtR), which reflect central adiposity, have been suggested to be superior to BMI in predicting CVD risk (37–39). This stems from the observation that ectopic body fat is related to a range of metabolic abnormalities, including decreased glucose tolerance, reduced insulin sensitivity, and adverse lipid profiles that are, in turn, risk factors for type II diabetes and CVD.

Current evidence is conflicting on the best measure of obesity for predicting adverse long-term outcomes; for diabetes, measures of central obesity were more strongly associated with risk compared with BMI, whereas this is not the case for hypertension and dyslipidemia where the relationships with BMI, WC, and WHR are similar.

For cardiovascular outcomes among the obese, the evidence again is conflicting except for the INTERHEART study, suggesting that the magnitude of the relationships between BMI and central obesity with cardiovascular mortality is broadly consistent. However, much of the evidence is based on cross-sectional studies, and there is a clear need for further data from large-scale prospective longitudinal studies (40).

Effects on pregnancy

First trimester maternal obesity has more than doubled from 7.6% to 15.6% over the last 19 years (p < 0.001) (41).

Maternal obesity has significant implications for the health of women and their babies, including the risk of maternal death. Obesity is independently associated with an increased risk of dying from specific pregnancy complications (42). The MMBRACE (2017) report cites a maternal death rate of 9.02 per 100,000 maternities (95% confidence interval [CI] 7.85–10.31). Over half of the women who died were overweight or obese in 2011–2013 and a third in 2012–2014 as per the report.

Women with a BMI ≥30 and their babies are at risk of the following complications when compared to women with a healthy pre-pregnancy weight (Table 8.2).

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