The American College of Obstetricians and Gynecologists (ACOG) noted that the dramatic increase in obesity in the United States in the later part of the 20th century is reflected among childbearing women.¹ The National Health and Nutrition Examination Survey of obesity among adults, conducted in 2011 to 2012, found that 36.1% of adult women were obese; among African American women, the figure reached 56.6%, and among Hispanic women, it was 44.4%.² Those alarming statistics not only have important clinical significance but also reflect social, political, and ecological trends that provide the context to and contribute as risk factors to poor pregnancy outcomes.

In this chapter, I use two social science conceptual paradigms to understand obesity in pregnancy: social determinants and stigma. The chapter reviews published studies, national-level data, as well as studies and data from Syracuse, New York, conducted by my colleagues and me.

The most useful definition of social determinants of health is that of the World Health Organization: “the causes of the causes.”³ Social determinants, in this model, are political, societal, and ecological risk factors that increase the likelihood of disease. They can be distinguished from clinical causes of ill health, in that clinical causes address immediate biological etiologies, whereas social determinants address a broader context of risk that takes place at an earlier phase in the condition. In the case of obesity, for example, the Centers for Disease Control and Prevention succinctly stated the clinical etiologies as “eating too many calories and not getting enough physical activity.”⁴ The social determinants approach, looking at the broader context in which obesity occurs, takes into account the factors that lead to poor diet or inadequate exercise or even altered metabolism. Understanding those social factors helps to explain why disadvantaged populations experience greater obesity and with it obesity-related health conditions.

A growing literature considers the influence of food deserts on health and obesity. Food deserts are geographical areas with few or no retail sources of fresh produce, low-fat dairy, or other healthful food.⁵ In many US cities, urban renewal led to the displacement of low-income residents, movement of wealthier people to the suburbs, and closing of neighborhood food markets. What food outlets remain in many communities are corner stores mostly selling lottery tickets, cigarettes, and malt liquor, as well as fast food franchises.⁶

In Syracuse, New York, our research team found food deserts to be significantly associated with intrauterine growth restriction (IUGR).⁷ Women residing during pregnancy in census tracts without access to full-service grocery markets had nearly four times the rate of IUGR, compared with those living in areas with greater access to healthy food and controlling for both race and Medicaid insurance as a proxy for poverty. In a subsequent analysis, which included all Syracuse births for a 2.25-year period among woman delivering at the largest birth hospital, the zip codes in which women with the highest proportion of obesity (>27% vs. <21%) lived were also the locations of food deserts.

The absence of healthy food does not mean an intake of fewer calories. Instead, residents of impoverished inner cities with food deserts often make up for the lack of fresh produce with prepared food, which is loaded with sodium, refined carbohydrates, unhealthy fat, and preservatives.⁸ In a teaching exercise with medical students at Upstate Medical University, we paired the students with adult patients with chronic disease and asked the students to shop for food with their patients. One of the student teams reported that their patient, who was obese and had type 2 diabetes, with poor circulation and renal complications, shopped for food at the local dollar store. The dollar store sold boxed and canned prepared food, but no fresh produce. The paradox of an overabundance of total calories, combined with malnutrition of micronutrients, may explain the finding that obese women have higher rates of neural tube defects because a major risk factor for neural tube defects is inadequate folic acid intake in the months prior to conception.⁹

Neighborhood violence is a second social determinant of obesity in pregnant women. Violent neighborhoods make it unsafe to walk for exercise and make parents reluctant to have their children play outside.⁶ A study conducted in Dallas, Texas, reported that women who perceived their neighborhood environment unfavorably, a measure that included sidewalks, housing quality, and violence, had higher waist circumferences and BMIs.¹⁰ Similarly, a study on prepregnancy BMIs among Latinas in Phoenix, Arizona, concluded that the neighborhood physical and social characteristics, including safety and motor vehicle traffic, provided conditions that increased the likelihood of obesity.¹¹

A third social determinant of obesity among pregnant women relates to the ingestion of specific substances. While it is true that no one factor has caused the dramatic rise in obesity, numerous authors argued that sweetened soda ingestion, and the intake of other sugar-sweetened beverages, accounts for a disproportionate amount of the recent population-wide BMI increase.^{12,13,14,15,16} Endocrinologist and pediatrician Robert Lustig pointed to the contemporary habit of consuming sweetened drinks as a key factor in promoting obesity.¹⁷ Daily consumption of highly sweetened liquid is unusual in human diets historically and cross culturally. Many cultures prepare special highly sweetened foods, usually for celebratory feasts, but such treats usually also contain protein, fat, and fiber, nutrients that slow the metabolic uptake of the sugar, honey, or fructose in the food. They are also consumed in discrete servings, in contrast to sweetened drinks, which may be sipped throughout the day. In contrast, Lustig claimed that our “obesogenic” environment of sugar-laden fast food and highly sweetened drinks leads to insulin and leptin resistance, blunting satiety and decreasing physical activity.¹⁸

The Centers for Disease Control and Prevention assessed the price increase of a variety of foods between 1982 and 2002. Costs of fruits and vegetables rose by 258% during that period, whereas the cost of sweetened soft drinks only increased by 26%.¹⁹ The reason that soft drinks remained cheaper than healthy alternatives is that the United States subsidizes corn growers, between 1985 and 2013 totaling $84.4 billion.²⁰ Corn subsidies allow high-fructose corn syrup to be marketed more cheaply than would be the case without subsidies, resulting in ever-larger servings.²¹ In 1995, for example, a serving of soda came to 7 ounces, whereas our contemporary “big gulps” reach 40 ounces or more.¹⁹ Consumption of sweetened soda tripled in the past two decades. A recent study found that over 27% of New York City adult residents consumed 12 ounces of sweetened soda daily, the equivalent of 10 teaspoons of sugar.¹⁵

Faculty at Upstate Medical University conducted a pilot study of the ingestion of sweetened soda and other beverages among pregnant women.²² In our review of MEDLINE^® studies, we could not identify any other such studies. The study’s initial findings were that many women drank fewer sweetened beverages than prior to pregnancy, often because such drinks worsened their reflux, and some women consumed large quantities, even liters of soda. The study’s recommendation was that antenatal care providers, and nutritionists providing education to pregnant women, ask about their clients’ consumption of sweetened beverages.

A fourth social determinant of obesity, the psychosocial stress associated with exposure to racism, has been identified as a potential risk factor for elevated visceral fat deposition.^23,24,25,26 The hypothesized biological pathway for stress to lead to abdominal obesity is via elevated cortisol, which in turn increases fat deposition and appetite. Research among Afro Caribbean women found their perceived stress due to internalized racism to be significantly associated with waist circumference and with elevated salivary cortisol.²⁷ Two additional studies found self-reported discrimination to be a risk factor for adiposity.²⁸ The deleterious effects of such exposure to discrimination have been identified as a risk factor to explain the disproportionate amount of cardiac disease among African Americans.²⁹ Visceral abdominal fat (VAF) is itself a risk factor for poor glucose control during pregnancy.³⁰ A study that measured the depth of VAF among pregnant women at 11 and 14 weeks’ gestation, which they subsequently compared with the women’s 2-hour glucose tolerance tests at 16 and 22 weeks, found VAF to account for 42% of the variance in insulin resistance.

Obesity itself may be a social determinant of elevated teen pregnancy, via the mechanism of early puberty.⁶ Increased body weight among prepubescent girls appears to be a driving factor in the alarming drop in the age of menarche during the 20th century.³¹ Prior to the modern era, growing girls in many cultures endured periodic food shortage due to drought, crop failures, or even the yearly cycle in which stored food was consumed sparingly during the winter prior to modern food storage and refrigeration. Female food intake in many traditional societies was also limited by cultural beliefs that restricted their access to certain foods or that religiously prescribed fasts.^32,33 Without antibiotics and vaccines, children suffered lingering illnesses with attendant anorexia, diarrhea, and months of growth interruption. The advent of puberty, in those conditions, fell late into the teen years. Philippine Island hunter-gatherer girls, for example, living in similar premodern conditions in the 1980s when they were studied,³⁴ began menstruating at age 17. In France in 1840, the average age of menarche was over 15 years, dropping by 2000 to 12.6 years.³⁵

Evolutionary scientists still disagree on the precise factors contributing to this preternatural sexual maturation, but most credit some aspect of the present-day food abundance and increased body weight. Frisch,³⁶ in 1993, claimed in her “critical fat hypothesis” that human females needed a precise set point of fat deposits to ovulate. Later studies concluded that there is no precise set point of body weight or percentage of body fat that leads to the first menstruation in all populations.³⁷

Nevertheless, body weight,³⁸ fat deposition, and the specific area of fat deposition³⁹ have all been demonstrated to precede first menstruation. For example, a longitudinal cohort study of Chinese girls that began at age 8.5 compared three groups: underweight, normal weight, and obese.⁴⁰ The obese girls experienced earlier breast maturation (measured as breast II development) and menarche than the other two groups. A study in New Zealand found increased adiposity to be associated with earlier menarche and decreased insulin sensitivity.⁴¹ Another study, looking at nationwide cross-sectional data from the United States, remarked on the consistent finding that girls with higher BMIs reached puberty earlier.⁴² The authors of that study, reviewing rodent studies on puberty and fat suggested that rising leptin may be the key trigger precipitating the onset of puberty. So, childhood obesity that leads to earlier puberty results in a longer period of time at which the young girls are fertile. Recent studies of adolescent brain development showed that the understanding of the consequences of their behavior, predicting risks, and controlling emotions develops during the teen years.⁴³ Early pubertal sexual maturity, in our modern era, now often precedes sufficient cognitive development to make wise choices regarding sexuality and reproduction.