Historically, social deprivation and poverty have been associated with hunger and starvation. During the last 2 decades in the postindustrialized world, poverty has become more associated with obesity than starvation.1 When obesity was initially recognized as increasing in 1990, no state in the United States (US) had an obesity prevalence of 15% or greater.2 In 2016, the prevalence of obesity in women aged 20 to 39 years in the United States was 36.5%.3 Worldwide, obesity has almost tripled since 1975, with obesity-related disease killing more people than undernutrition.1
Obesity affects some racial/ethnic groups more than others. Hispanic and non-Hispanic black women have the highest age-adjusted prevalence of obesity (50.6% and 54.8%), followed by non-Hispanic white women (38.0%) and non-Hispanic Asian women (14.8%).3 Obesity is increasingly recognized as an adipose organ disease with health compromising effects across the life span including the perinatal period with risks to both mother and newborn (see Table 1).3-5
When conditions affect more than half a population, causation needs to be sought beyond personal choices by considering systemic social and environmental contributions to health. This review examines new concepts in obesity and associations between socioeconomic disparities in education, income, health, and obesity, concluding with individual and population-targeted nursing actions to ameliorate obesity-related perinatal morbidities.
OBESITY AS AN ORGAN DISEASE
Obesity originally was attributed to excess caloric intake without sufficient physical activity for energy use with white adipose tissue serving as the storage depot for excess energy.3 Responsibility for excess weight was viewed as a personal lack of discipline in eating and physical activity. Newer research in metabolism, psychoneuroimmunology, and adipose has moved the definition of obesity from a set of character faults to the definition promoted by the Obesity Society: "a chronic, relapsing, multifactorial, neurobehavioral disease, wherein an increase in body fat promotes adipose tissue dysfunction and abnormal fat mass physical forces, resulting in adverse metabolic, biomechanical, and psychosocial health consequences."6 This newer definition allows for the inclusion of multiple potential contributors to obesity including social disparities in economics, education, nutrition, and the environment.
Although obesity is defined as a body mass index (BMI) of 30 or greater (BMI = weight [kg]/[height (m)]2), there is debate about BMI as an appropriate measure of adiposity because for any BMI unit, the composition of adipose and muscle varies between people of the same sex across race and ethnic groups.1,2,7 Waist circumference is a better predictor of future obesity-related morbidity7; however, waist circumference changes dramatically in pregnancy. In addition, the definition of obesity using waist circumference varies by race with a waist circumference of 35 inches or greater in Caucasian females but 31 inches or greater in Asian females indicating obesity.3,7 Therefore, BMI at the first prenatal visit is the measurement used to define obesity in perinatal research.8
White adipose tissue
White and brown adipose tissues are endocrine organs with multiple metabolic functions. Brown adipose, found mainly in newborns, produces heat when metabolized, a protective factor during cold exposure. Like the dermis, white adipose tissue is widely distributed throughout the body and might be the largest hormone-producing tissue secreting endocrine, paracrine, and autocrine signals.9 White adipose is rich in macrophages that are the source of tumor necrosis factor [alpha] and interleukin-6. Production of proinflammatory adipocytokines is a major contributor to the chronic inflammatory state found in obesity and likely contributes to obesity-related diabetes, atherosclerosis, hypertension, and perinatal morbidities and mortality.9,10Table 2 outlines factors secreted by white adipose tissue, functions, and the main sites of production.
Epigenetics of obesity
Barker developed the fetal origins hypothesis in the early 1990s, using evidence from birth records linked to adult health records to demonstrate that adult diseases including diabetes, hypertension, heart disease, and stroke are the sequelae of poor maternal health and in utero undernourishment.11 Fetal programming in utero has been hypothesized to start with maternal undernutrition and calorie restriction that reduce placental growth and function causing decreased glucose oxidation with increased amino acid and lactate oxidation.12 Endocrine changes include increased cortisol production with decreased production of insulin, insulin-like growth factor-1, and growth hormone.12 This undernutrition and decreased fetal growth programs the child for insulin resistance, metabolic syndrome, hypertension, type 2 diabetes, and heart disease. Counterintuitively, low birth weight newborns catch up on growth if exposed to excess calories and the programmed metabolic dysregulation pushes the child toward obesity.11,12
Research since Barker has shown that genes can be dysregulated by methylation producing novel phenotypes, suggesting that programming may occur at the cellular level.13,14 Fetal programming in utero is now conceptualized as epigenetic changes, changes in gene expression that are independent of changes in deoxyribonucleic acid. The preconception use of folic acid supplementation to prevent neural tube defects is an example of a bioactive diet that provides beneficial epigenetic changes. Women with obesity have higher circulating levels of the adipose-secreted molecules in ovarian follicular fluid that may produce epigenetic changes in ova. The same processes may affect sperm and seminal fluid, producing the reduced fertility seen in men with obesity.14
Epigenetic changes may occur in ova, sperm, or the zygote, and then be replicated through cell division. Ova, sperm, and the developing blastocyst are adaptive and primed for success in the immediate prepregnancy, undernourished environment.15 If the child enters a new environment rich in calories, the adaptive gene becomes maladaptive and may prime the child for obesity. Phenotypic changes related to deoxyribonucleic acid methylation have been shown to persist across generations and might be a partial explanation for the dramatic rise in obesity during the last 3 decades.15
Maternal smoking and obesity
Exposure to maternal smoking in utero has been associated with at least a 30% increase in risk for adult obesity.16,17 Cigarette smoking has declined substantially in the United States; however, the prevalence of smoking remains higher in lower-income groups.18 A study in which 26.1% of nurses reported smoking during pregnancy found a significant association between maternal smoking during pregnancy and overweight and obesity in adulthood with the risk of overweight and obesity increasing with the number of cigarettes smoked daily.19 Children of women who stopped smoking at the start of pregnancy did not have an increased risk for adult overweight and obesity. Tobacco-exposed, low birth weight newborns may exhibit the growth catch-up phenomena described by Barker.11
Obesity and the microbiome
The newborn is colonized by the maternal vaginal microbiome during birth. Emerging evidence reveals that the gut microbiome has nutrient and satiety sensing and signaling properties, along with roles in energy harvesting and inflammatory response modulation.20-24 A cascade of gut reactions begins with a high-carbohydrate, high-fat diet that favors changes in the gut microbiome and initiates an inflammatory environment that allows for increased permeability between intestinal cells.20,21 Adipose tissue cytokines increase this chronic, low-level inflammation changing gut-to-brain signaling that stimulates hyperphagia and increases obesity.20,21 Human and animal studies have shown that those with obesity have gut microbiomes that are both different in bacterial composition and diversity compared with the microbiomes of those with normal weights.22,23 Maternal prenatal nutrition altering the gut microbiome may cause histone modification or deoxyribonucleic acid methylation epigenetic changes or alter the fetal gut microbiome provoking obesity-stimulating epigenetic changes.25
CONTRIBUTION OF SOCIAL DISPARITIES TO OBESITY
Although individual dietary and activity choices are under personal agency, those choices are limited by social and environmental constraints. Disparities in available education, employment, income, healthcare access, the lived and built environment, and available nutrition shape individual choices and epigenetic inheritance (see Figure 1). Understanding the contributions of social disparities to obesity broadens opportunities for health-improving interventions, moving these from the individual to community level.
Socioeconomic disparities
Racism
Race is a controversial sociopolitical construct that categorizes people by phenotype. Race as a proxy for genetic variation is investigated for its links to disease risk. Ethnicity is a broader category that combines racial phenotypes with cultural variables including shared history, language, religion, and dietary customs. Racism, the discrimination and unequal treatment of individuals of racial and ethnic groups in the United States in almost all aspects of daily life, is a chronic life stressor that can have health consequences.26 The stress of racism erodes health through wear and tear according to the life-course perspective.26 Other hypotheses implicate chronic activation of the hypothalamic-pituitary-adrenal axis by stress as a cause of disease. Regardless of explanatory model, the stress of racism may cause epigenetic changes.26 The socioeconomic inequalities imposed by racism systematically expose groups to other obesity-linked inequalities, including lower education; reduced access to healthcare; lower health literacy; stressful, low-wage work; unsafe neighborhoods; environmental pollutants; and food deserts.
Using interview data from a probability sample of 1870 including non-Hispanic white, non-Hispanic black, and Hispanic women, investigators linked the concepts of racism and vigilance (chronic attention to potential prejudice, discrimination, and racism) with increased BMI and waist circumference.27 Black women had higher vigilance scores than Hispanic or white women (30%, 16%, and 9%, respectively). Waist circumference patterns and BMI mirrored vigilance findings with black women and Hispanic women having wider mean waist circumferences than white women (9.0 cm and 6.4 cm larger). The authors proposed that consumption of obesogenic foods and the subsequent release of mood-elevating neurohormones may be used as a stress-coping mechanism that accounts for elevated BMI and larger waist circumferences.27,28 Alternatively, the stress of chronic vigilance may activate the hypothalamic-pituitary-adrenal axis increasing adipose deposition.
Police maltreatment, a frequent cause of vigilance, was examined in another study comparing personal or vicarious unfair treatment by police to waist circumference in a sample of black and white women.29 Individuals experiencing vicarious unfair treatment by police had waist circumferences that were approximately 2 inches larger than those who did not, leading authors to conclude that discriminatory policing is a potential contributor to racial disparities in health.29
Education
Disparities exist in access to education and the quality of public education in the United States, with obesity rates increasing as years of completed education decrease across racial and ethnic groups.30,31 An analysis of the relationship of obesity and education using 2011-2014 National Health and Nutrition Examination Survey data revealed a 39% rate in the lowest income group but a 31% obesity rate in the highest income group.31 Educational disparities may decrease health literacy reducing attention and comprehension to weight management education. Researchers analyzed 2007-2014 National Health and Nutrition Examination Survey data for usage of calorie labeling in restaurant menus finding that usage in all groups increased with increasing education and income.32 Limited or poor-quality education is linked with reduced employment opportunity and lower income.30-32 The higher obesity rates of women may be associated with multiple disparities in education, employment, and income.
Employment
Low-wage employment opportunities are more often filled by individuals from racial and ethnic minorities. A study of US transit workers found that African American and Hispanic females had higher obesity rates than men or other female operators.33 Work stresses, including 10- to 15-hour shifts and the constant vigilance required during driving, in addition to the intersecting social identities of lower social class and minority women, were thought to augment hypothalamic dysfunction contributing to the higher obesity rates of minority women.33
Shift work requiring changes in sleep/wake cycles alters the circadian rhythms of key metabolic hormones such as leptin and insulin and has been associated with obesity.34 A systematic review of 16 cross-sectional studies investigating short sleep, obesity, and metabolic changes found consistent associations between short sleep and higher consumption of poor nutritional quality foods with high fat content and fewer fruits and vegetables.34 Increased intake may result from increased waking hours for snacking and meals.34
Access to healthcare
Healthcare insurance, the key to healthcare access, is still tied to employment in the United States. Black and Asian individuals are more likely than Hispanic or white individuals to be unemployed longer than 27 weeks,35 thus limiting access to healthcare, especially preventative healthcare education. A 2-decade increase in part-time work, stagnation in wages, and changes in types of employment has eroded employer-sponsored health coverage and access to healthcare.36 Provisions in the Affordable Care Act were targeted at reducing the cost of providing health insurance for employers; however, recent legislative changes have limited the impact of the Affordable Care Act in increasing healthcare access.36
Nutritional disparities
Food quality and quantity
A major constraint on personal nutrition is the cost of food. Low-wage earners have decreased ability to purchase fruits, vegetables, and whole gain foods as those foods cost more per calorie than processed, calorie-dense foods and sugared beverages.37,38 A multinational literature review of food prices and diet quality found that individuals with reduced incomes stretched food dollars by meeting energy needs at the lowest cost per calorie, processed foods regardless of the overall nutritional value. Processed foods were also viewed as easier to prepare and more palatable.38 Living in a food desert (a residential neighborhood with few full-scale markets for affordable and nutritious foods and more convenience stores) has been linked to increased risk for obesity.35 Convenience stores typically sell calorie-dense, more affordable, low-nutrition foods with long shelf lives, thus making an obesogenic diet more available.37,38
Another study of food purchases explored the concepts of food security (availability and access to sufficient, safe, and nutritious foods at all times) and food deserts related to income using the United States Department of Agriculture's 2012-2013 Food Acquisition and Purchase Survey.39 The nationally representative sample found that having a supermarket less than 1 mile from home was not associated with food security but access to an automobile was. Most households used automobiles to travel to markets with the lowest cost foods, often bypassing closer, more nutritious but expensive food sources.
Infant feeding
Nutritional disparities may begin immediately after birth. Obesity has been linked to delayed lactogenesis II and latch difficulties, eroding maternal confidence in breastfeeding.5,40 Infants of women with pregestational obesity are at risk for early formula supplementation or weaning with early introduction of juices and solids such as cereal.41,42 The epigenetic potential of these feeding behaviors is unknown. Two studies have examined early infant feeding in Hispanic and African American families with low incomes, finding that rates of age-inappropriate feeding were high.41,42 Early supplemental feeding may confuse infant gut and hormonal signals for hunger and satiety, increasing the risk for childhood obesity. Research also found parenting attitudes about feeding that put children at risk for obesity including beliefs that parents knew when infants were hungry regardless of newborn cues.41 Powerful barriers to following national infant feeding guidelines have also been identified including single parenting, low income, and depression.42
Environmental disparities
Unsafe neighborhoods
The built environment is considered a contributor to sedentary behavior and obesity. Other environmental factors such as neighborhood safety and pollutants may also contribute to obesity. One national study found that non-Hispanic black and Hispanic individuals reported neighborhood crime and animals as barriers to safe walking significantly more often than white individuals.43 Women also consider the potential for sexual violence when perceiving safety in neighborhoods.44 Those living in neighborhoods perceived as unsafe may spend more time indoors in sedentary activities such as television watching.
Environmental pollutants
Endocrine-disrupting chemical pollutants are pervasive in outdoor and indoor environments and can be ingested orally, inhaled, or absorbed through the skin. Endocrine-disrupting chemicals (EDCs) with known obesogenic potential include persistent organochlorines, bisphenol A (BPA), phthalates, polybrominated diphenylethers, parabens, and phytoestrogens. Obesogenic EDCs contained in plastics, can liners of canned foods, flame retardants, detergents, dental sealants, pesticides, and herbicides affect adipose control through interfering with steroid and thyroid hormone function, altering insulin sensitivity, increasing adipose cell number and size, and favoring adipose deposition.45,46 Adipose stores of EDCs can be mobilized into circulation during weight loss and lactation.46 The summative effect of endocrine disruption may be alterations in the hormonal control of satiety and hunger.45
Disparities in available housing concentrate individuals with low incomes and racial/ethnic minority groups in neighborhoods with higher levels of pollutants including EDCs.46 Sources include industrial waste and illegal dumping worsened by governmental failure to enforce environmental regulations.46 A study using National Health and Nutrition Examination Survey 2003-2006 data found that income was inversely related to BPA levels with low income more related to BPA levels than race or ethnicity.47 Individuals with high food insecurity, particularly those using emergency food sources such as food pantries, where foods are packaged for long shelf lives in EDC-containing cans or plastic containers, had higher BPA levels than food secure participants.47
DISCUSSION
Although obesity places women at risk for numerous morbidities, most women with obese BMIs complete pregnancy and birth without complications.4,40,48,49 Recognition of the multiple contributors to obesity, including numerous social disparities that limit individual nutrition and activity choices, is the first step to improved care for women with obesity. Table 3 summarizes perinatal care measures for women with obesity.
The guidelines from the American College of Obstetricians and Gynecologist urge women to normalize BMI before attempting pregnancy4; however, weight loss programs of any kind have limited effectiveness.52 Black and Hispanic women have lower access to health insurance that would allow primary healthcare support for prenatal weight loss guidance.36 Calorie restriction alone is more effective than programs including a diet, psychological counseling, and physical activity.52 With many women perceiving neighborhoods to be unsafe for physical activity,43,44 the most effective preconception therapies may be epigenetic (those that create a better environment for ova and sperm), reduced calorie diets with folic acid, vitamin B, and essential micronutrients supplementation that avoid sources of toxic EDCs such as those in plastic containers and cans.53,54 Fresh fruits, vegetables, whole grain carbohydrates, and other low glycemic index foods are examples of foods for epigenetic diets. Epigenetic diets may optimize the follicular and intrauterine environments limiting epigenetic changes that favor childhood and later adult obesity.53 Assisting women to plan for nutritious meals and appropriate weight gain is an essential component of prenatal care. Gestational weight gain limited to 11 to 20 lb for women with prepregnancy obesity is associated with improved perinatal outcomes.4 Nurses must be politically active in supporting federal, state, and community food distribution policies. Examples of these include the Women's, Infants' and Children's Supplemental Nutrition Program, laws requiring nutrition information on menus, and zoning laws that favor supermarkets over convenience stores.
Care measures for obesity-related morbidities do not differ between women of normal or obese BMIs. Diabetes and hypertension management remain the same regardless of BMI; however, obesity-related perinatal morbidities that fall into 2 categories, those caused by inflammation and those caused by hormone resistance, require special consideration. Leptin sensitivity, like insulin sensitivity, is reduced in obesity.55 High leptin and visfatin levels limit the effectiveness of oxytocin, reducing myometrial contractions.55 This is a likely factor in the higher incidence of prolonged pregnancies and the longer labors in obesity.55 Because of the tocolytic effect of leptin, mechanical cervical ripening may be more effective than use of prostaglandins.50 Most women will benefit from vigilant patience while awaiting the onset of labor and during prolonged labors.48,49 Patience may include use of a longer labor curve; however, no partograms adjusted for BMI have been developed. Because of the high rate of uterine atony with postpartum hemorrhage associated with obesity,48 active management of the third stage with delayed cord clamping can be discussed with women during the third trimester and recommended. High leptin levels may also reduce the effectiveness of oxytocin on myoepithelial cells involved in the milk ejection reflex contributing to delayed lactogenesis II.5 All measures that facilitate early breastfeeding support women with obese BMIs while lactation is established.5
The chronic, systemic inflammation associated with adipose dysfunction increases the risk for postpartum deep vein thrombosis.4 As with others at risk for deep vein thrombosis, early postpartum ambulation is a key element of care.4 Alternating compression stockings and low-dose anticoagulation for 24 to 48 hours postpartum are also care considerations particularly postcesarean surgery.4 Blood glucose levels normalize immediately postpartum in women with obesity and gestational diabetes, but women remain at increased risk for future type 2 diabetes.51 Therefore, postpartum diabetes screening at 4 to 12 weeks is offered to women with obesity complicated by gestational diabetes.51
Future obesity research will need to examine increasing global experience with obesity-related morbidities at the individual and population levels to capture the effects of socioeconomic and environmental disparities on obesity. Epigenetic changes will need to be studied over generations to reveal stronger causal links with obesity. Finally, clinical practices meant to ameliorate obesity-related morbidities will need to be studied for effectiveness, safety, and patient satisfaction.
CONCLUSION
The research cited in this article involving socioeconomic disparities, the microbiome, EDCs, epigenetics, and links to obesity moves the focus of obesity prevention from the individual level to the community and national health policy levels. Other factors are yet to be discovered and may limit the applicability of this review. Black and Hispanic women coping with obesity and social disparities in education, employment, and the environment also suffer from the dual discriminations of obesity and racism. The most effective measures for reducing future population obesity will not be accomplished at the individual patient level but will involve reducing the socioeconomic disparities that underpin obesity. Environmental activism to reduce obesogenic pollutants seems far removed from nursing care but may be an important strategy in future weight optimization. Attempts to reduce the stress of living with racism, improve educational equity, and promote fair employment practices are long-range strategies for obesity reduction. As the most numerous healthcare providers in the United States, nurses can affect changes in obesity at the individual and population levels through targeted patient care and sustained sociopolitical action.
References