Global Health Complications of Obesity

Vadimsky.

Chapter 1

What is obesity?

Abstract

Today, obesity is a global epidemic that causes many different complications and chronic diseases. For the first time in history, the number of overweight or obese people is close to the number of underweight people. In the United States alone, costs for management of obesity reached $344 billion in 2018. This averages to more than $800 per person. A man or woman is considered to be obese when his or her body weight is 20% or more above normal weight for the individual’s height. The term obesity actually means excessive body fat, based upon body mass index, which compares weight to height. Obesity results in many chronic diseases that affect the health of patients and increase health-care costs.

Keywords

Obesity; chronic diseases; overweight; BMI; risk factors

Overview

Today, obesity is a global epidemic that causes many different complications and chronic diseases. For the first time in history, the number of overweight or obese people is close to the number of underweight people. In the United States alone, costs for management of obesity reached $344 billion in 2018. This averages to more than $800 per person. A man or woman is considered to be obese when his or her body weight is 20% or more above normal weight for the individual’s height. The term obesity actually means excessive body fat, based upon body mass index (BMI), which compares weight to height. Obesity results in many chronic diseases that affect the health of patients and increase health-care costs.

Overnutrition is a form of malnutrition. It is caused by excessive caloric and nutrient intake. This leads to becoming overweight and eventually, obese, both of which are classified based on BMI. This measures body composition, calculated by taking a person’s weight (in kilograms or pounds), and dividing it by his or her height (in meters or inches). It is important to understand that BMI does not adjust for body fat percentage. This means that people with significant muscle mass can be incorrectly described as overweight, when they actually are not. Since BMI does not measure levels of physical fitness, patients with poor cardiovascular endurance, regardless of BMI, are at risk for many poor health outcomes. Obesity is linked to an increased risk for type 2 diabetes, hypertension, heart disease, strokes, digestive disorders such as gallstones, back pain, hip and back arthritis, and several forms of cancer. Adult BMI has increased steadily in most countries over the past three decades.

Definition and measurement

Obesity is an abnormal increase in the proportion of adipocytes, mainly within the viscera and subcutaneous tissues of the body. It may be exogenous or endogenous. Hyperplastic obesity is caused by an increase in the number of fat cells in the increased adipose tissue mass. Hypertrophic obesity results from an increase in the size of fat cells in the increased adipose tissue mass. The term overweight is determined by a BMI of 25–29.9 kg/m², and obesity is determined by a BMI of 30 kg/m² or higher. Body fat distribution can be assessed by waist-to-hip ratios, with a ratio of greater than 1.0 for men and greater than 0.8 for women, signaling increased risk of obesity.

The guideline for the management of overweight and obesity in adults defines these conditions and gives recommendations on their evaluation and management, that is, based on scientific evidence. BMI is the recommended approach for categorizing weight relative to height for adults. Its formula is simple: weight in kilograms divided by height in square meters. The formula can also be calculated in pounds in inches, by having the weight in pounds divided by the height in square inches, multiplied by 703. Table 1.1 summarizes classification of overweight and obesity by using BMI.

Table 1.1

Interestingly, people who are classified as overweight may or may not appear to be excessively fat. Some adults are overweight because of increased muscle mass, as easily observed clinically. Generally, risks for developing fat-related health problems increase continuously as BMI exceeds 25. The new guidelines recommend use of waist circumference measurements for a more accurate understanding of each patient’s condition. For people in the overweight and class I obese categories, with a high-risk waist circumference, there must be discussion of lifestyle changes to improve health and result in weight loss. Some patients with a BMI of 27.0–29.9 develop significant metabolic complications, but these improve with weight loss. Therefore such patients are candidates for pharmacotherapy and other more aggressive treatments. For example, Asians are at risk for typical metabolic complications of obesity at lower BMI and waist circumferences than Caucasians, Hispanics, African Americans, and Pacific Islanders. The guideline for at-risk BMI in Asians is 23–24.

Comorbidities and future morbidities are of much higher incidence when the BMI is more than 30. With the three classifications of obesity, treatment differs. The US Food and Drug Administration currently recommends that pharmacotherapy be used as adjunct treatment for all obesity classifications, even if no medical complications are present. It is important to be familiar with these guidelines. Third-party insurance payers and supervising agencies use the guidelines in determining patients who are eligible for treatment benefits. Extreme obesity, over 40, is a key feature prompting consideration of bariatric surgery after medical treatments have failed. For class II obesity, bariatric surgery may be considered if medical treatments fail, and if severe and possibly life-threatening complications exist.

The latest guidelines suggest that previous waist circumference cutoff points of more than 40 in. for men and more than 35 in. for women indicate increased metabolic risks. However, relationships between waist circumference and disease risks are continuously progressive and have no obvious cutoff points. Therefore waist circumference should be measured in overweight and class I obese adults. When the waist circumference exceeds the cutoff points, there must be additional evaluation to detect other risk factors for cardiovascular disease. Class II or class III obese adults have a high enough risk so that waist circumference is not actually additionally important. The cutoff points for each overweight or obese classification apply to most people of European and African descent, but not Asians.

Epidemiology

Obesity is a global pandemic, and one of the most serious threats to public health. During the past 30 years the number of overweight and obese adults has increased dramatically (see Fig. 1.1). However, today, the increase in prevalence is slowing and becoming more consistent. In a 2009–10 study, prevalence of obesity was 35.8% in adult women and 35.5% in adult men. This showed no large change compared with the years 2003–08. As of 2016 a collection of studies revealed that the world population has added an average of 1.5 kg of weight per year, definitely signaling an obesity epidemic. It is estimated that there are now more than 640 million obese people around the world. This is higher than ever before in history and has also surpassed the number of people who are dangerously underweight. Fig. 1.2 shows a global map of adult obesity in 2016 and was obtained from the World Health Organization.

Focus on obesity in the United States

In the United States, more than one-third of adults are obese. This makes up 34.9% of the adult population, or about 112.7 million people. Approximately, one out of every five deaths are linked to obesity.

Figure 1.1 Global increases in average adult BMI between 1975 and 2014. BMI, Body mass index. Source: NCD Risk Factor Collaboration. Trends in Adult Body-Mass Index in 200 Countries From 1975 to 2014: A Pooled Analysis of 1698 Population-Based Measurement Studies With 19.2 Million Participants. Lancet 2016, 387, 1377–1396.

Figure 1.2 Global trends in adult obesity in 2016. Source: https://ourworldindata.org/obesity.

Differences in overweight or obese African Americans, Mexican Americans, and European Americans are large. The highest rates of overweight and obesity in the United States are seen in African American women and in Mexican Americans of both sexes. To be fully understood, however, this information must include the inverse relationship between socioeconomic status and obesity—especially in women. Females of lower socioeconomic classes are extremely likely, compared to those in higher socioeconomic classes, to be obese. This relationship lowers the racial differences in obesity prevalence. It is not known if remaining racial differences in obesity prevalence are because of genetic, social, or body makeup (constitutional) factors.

About 60% of men and 51% of women are overweight or obese in the United States, though more women than men are actually obese. Large differences exist in prevalence of obesity by age, race, and socioeconomic level (see Fig. 1.3). Prevalence of adult obesity rises steadily from 20 to 60 years of age and decreases in later years. Estimates are that nearly 75% of men aged 60–69 have a BMI higher than 25. Increases in mean BMI with aging is not as severe a threat to health as is a similar increase in younger people. Young adults with a 20.0–24.9 BMI have the lowest mortality rates, while BMI related to lowest morality rates is slightly above 25 for people in their 60s and 70s. Weight recommendations for each patient should be based on whether there are adverse health consequences present. In children or adolescents who are overweight or obese, there is a much earlier onset of complications. In the United States the percentage of high school students who were obese in 2017 is shown in Fig. 1.4. Health-care systems will eventually be overwhelmed by the long-term treatment of obesity-related complications, especially those that begin in younger patients. There are few accurate statistics on incidence concerning obesity, but some generalized facts are available. In most areas of the world, years lost to disability from obesity range between 15.5 and 22. Obesity contributes to 120 million disability-adjusted life years lost. The cost impacts of obesity, in the United States alone, range between $147 and $210 billion annually. There are now accurate cost impact statistics for all countries.

Figure 1.3 Obese people. Source: Photographed by the author.

Figure 1.4 The percentage of US high-school students with obesity in 2017. Source: https://www.cdc.gov/healthyschools/obesity/obesity-youth.htm.

Etiology and risk factors

Obesity is a direct result of a sedentary lifestyle and the chronic ingestion of excess calories. Many experts have ruled out a genetic basis for the obesity epidemic. This is based on the fast global rise in its prevalence. The gene pool of the population could not have changed so much in such a short time period. Genetics influence about 40%–70% of obesity cases. Obesity has also occurred because of environmental factors interacting with susceptible genes. Therefore research has mostly focused on social and environmental factors, referring to components influencing dietary intake and physical activity.

Other possible contributors to obesity include dietary components, age, gender, ethnicity, longevity, maternal influences in the perinatal period, emotional stress, depression, sleep disturbances, adiposity rebound, fat cell dynamics, food access and marketing, automation, mechanization, urbanization, pollutants with endocrine-disrupting effects, reproduction between individuals with similar phenotypes, and pharmaceuticals affecting weight. Examples of similar phenotypes include body size, skin color or pigment, and age. Assortative mating is the term used to describe this reproduction, which can increase genetic relatedness within families.

Many other factors increase the predisposition to obesity. These factors include tumors, Cushing syndrome, and hypothyroidism. About 15% of women permanently gain 20 or more pounds with each pregnancy. Insufficient sleep, of less than 6–8 hours per night, can cause weight gain via changing levels of hunger-promoting hormones. Weight-causing drugs include corticosteroids, lithium, traditional antidepressants, benzodiazepines, anticonvulsants, thiazolidinediones, beta-blockers, and antipsychotic drugs. Less commonly, weight gain is caused by brain damage from a craniopharyngioma, or an infection—especially one that affects the hypothalamus. These factors can stimulate consumption of excess calories. A pancreatic tumor can result in hyperinsulinism, increasing weight. Cushing syndrome can cause hypercortisolism, causing mostly abdominal obesity. Rarely, hypothyroidism is a cause of substantial weight gain.

There are also at least two eating disorders associated with obesity. Binge eating disorder involves consuming large amounts of food quickly, with a subjective sense of loss of control during binging, followed by distress. This disorder does not include compensatory behaviors such as vomiting. About 3.5% of women and 2% of men have binge eating disorder. Also, about 10%–20% of people entering weight reduction programs have the disorder. Their obesity is usually extreme. Large amounts of weight are often gained or lost, and there are significant psychological disturbances.

Night-eating syndrome involves anorexia in the morning, hyperphagia in the evening, and insomnia, often with eating in the middle of the night. More than 25%–50% of daily food intake occurs after the evening meal. Approximately, 10% of people entering treatment for severe obesity may have this disorder. In rare cases a similar disorder is brought about by hypnotic medications. Similar but less extreme eating patterns are believed to cause excess weight gain in many people. The risk factors of obesity also include modifiable and nonmodifiable components. Therefor obesity results from behavioral, environmental, genetic, and sociocultural factors. Table 1.2 summarizes the risk factors of obesity.

Focus on meat in the diet

Recent studies recommend that red beat, bacon, or sausage should only be consumed once per week, in order to reduce the likelihood of heart disease. Other meat sources, such as fish and chicken, are healthier choices.

Table 1.2

Genetics of obesity

It is well known that obesity runs in families. Family members often share similar environments and diet as well as exercise patterns. Evidence reflects as significant genetic impact upon body mass and obesity. There are three broad categories of genetic factors influencing obesity: monogenic forms, syndromic forms, and polygenic forms. Monogenic forms of obesity are due to rare, single-gene mutations. This may cause key hormone deficiencies regulating appetite and metabolism. The involved hormones include leptin and melanocortin. Usually, these gene mutations are associated with increased appetite and not with reduced energy expenditure.

Syndromic forms of obesity are also rare, but there are 30 different types. They occur from discrete genetic defects or from chromosomal abnormalities. Syndromic forms may cause dimorphic features, mental impairment, and developmental abnormalities such as Alstrom syndrome, Prader–Willi syndrome, Laurence–Moon–Biedl syndrome, and fragile X syndrome.

Polygenic forms of obesity occur from multiple gene effects. These have been seen in many dizygotic and monozygotic twins, parents, siblings, offspring, adoptees and adoptive parents, and those with extended pedigrees. Such individuals have strong genetic and heritable contributions to adiposity, including BMI, body fat, waist circumference, and fat mass.

However, combined effects of all identified genetic contributions make up less than 1% of the variance in BMI. This reveals significant environmental effects along with the polygenic nature of susceptibility to obesity. The heritability of obesity traits is the percent of individual variation of the trait that is explainable by inherited factors. Genetic studies in various populations have shown that 40%–70% of variability in body mass is heritable. A study of twins in Sweden showed that heritability of BMI was 70% for men and 66% for women. Regardless, these studies are limited by their ability to separate variability caused by genotype, via environmental interaction—since human genotypes cannot be replicated and studied in different environments.

Today’s environment may be mismatched with the thrifty genes seen in the past when food sources were not as predictable. This hypothesis was initiated to explain how genes that predisposed people to diabetes occurred. Geneticist James Neel suggested that thrifty genes were advantageous in previous times but became unneeded today. Thrifty genes allow humans to collect and process food, to deposit fat in times of food abundance, to be used later for energy when food is not as plentiful. This idea was expanded to evaluate obesity. The thrifty genotype hypothesis states that the genes of the past, which helped survive famines, are now challenged because food is plentiful consistently.

The heritability of BMI is approximately 66%. Genetics may affect the numerous signaling molecules and receptors that are used by areas of the hypothalamus and glycemic index tract for regulation of food intake. Genetic factors are either inherited or develop from in utero conditions described as genetic imprinting. In rare cases, obesity results from abnormal amounts of peptides such as leptin that regulate food intake, or abnormalities of the melanocortin-4 receptor. Genetics also regulate the expenditure of energy. This includes the basic metabolic rate, diet-related thermogenesis, and nonvoluntary thermogenesis that is related to physical activity. Genetic factors may have more effect upon body fat distribution—especially abdominal fat, which increases risks of developing metabolic syndrome—than on the amount of body fat.

Environmental factors contributing to obesity

Environmental factors influence energy intake and expenditure directly or indirectly. Therefore obesity is linked by food marketing strategies (especially to children) and the round-the-clock availability of cheap foods that are convenient to consume. These foods are usually energy-dense, high in fat and sugar, extremely processed, contain large portions, and are ready-to-eat. Excess calorie consumption and obesity has developed from increases in portion sizes over history. In the 1970s, portion sizes increased dramatically but then became even more excessive in the 1980s with the advent of fast food chains offering huge amounts of food in each meal. Total energy intake increases with larger portion sizes. Super-sized portions have developed mostly because of the public wanting more for their money. Larger portions mean more calories. A typical 64-oz soft drink contains nearly 800 cal—this is about half the daily energy requirements for most children and adolescents.

Environmental factors influence physical activity and the expenditure of energy. Our built environments either discourage, or less often, encourage physical activity. In urban settings, people usually rely more on cars and other motorized methods of transportations. People often drive for long distances to get to and from work. There may be a lack of areas to walk, run, bicycle, or play. More streetlights, sidewalks, and other urban designs often replace playgrounds, parks, and trails. In most businesses, automation and mechanization have reduced physical activity requirements. This is true for people of all ages. Physical activity requirements in school have declined from about 45% of the school day to about 25%. Many public schools have reduced or eliminated physical education classes.

Only about 20%–30% of Americans exercise at the correct frequency, intensity, or deration. This has not changed greatly over recent decades. Though it is easier to access devices to count daily steps and detect body motion, there are no solid studies about how these tools have helped in increasing physical activity. One study suggested that between 1982 and 1992, changes in workplaces reduced energy expenditure by about 50 kcal/day, and this has probably worsened over time. Laborsaving devices at work and in the home, as well as in public areas, result in us sitting for more time during the day. These include drive-through lanes, escalators, remote controls, and all computer activities. Walking has generally decreased while driving has generally increased.

Our behaviors have increased in their sedentary qualities, such as the use of computers, video games, and television. Children and adolescents are simply moving less and sitting more. Often, as these activities are occurring, the individual is consuming snack foods and drinking sweetened beverages. Psychological factors also influence how food affects energy intake. Some people consciously limit food intake to control weight, feelings of hunger, or the tendency to overeat at certain times. Between individual people, these factors modify how varieties and portion sizes of foods affect eating. Social situations in which food is eaten, and emotional states, can also affect food intake.

As of 2010, more than 43 million children were overweight throughout the world. This is more than double the amount (20 million) in 2005—just 5 years. Rates of obesity in developed countries are double that of developing countries, but developing countries have many more children affected. It is estimated that there are more than 35 million overweight or obese preschoolers in developing countries, but only over 8 million in developed countries. In the United States the sharp rise in childhood obesity resembles the increase in adult obesity. In 1990 prevalence of childhood obesity was not greater than 15% in any participating state, but by 2010, no state had prevalence less than 20%. Fig. 1.5 shows the Centers for Disease Control and Prevention’s (CDC’s) figures on childhood obesity in the United States for different age groups and also contrasts differences between boys and girls.

Figure 1.5 Prevalence of obesity in children 2–19 years of age, by sex and age, in the United States 2015–16. Source: https://commons.wikimedia.org/wiki/File:CDC_Prevalence_of_Childhood_Obesity.jpg.

Recent CDC data show that childhood obesity in the United States has risen from nearly 14% in 1999 to more than 18% in 2016. During this period, obesity rose 33% in the 2–19 age group. Prevalence of severe obesity has remained consistently high in the past 10 years (6.3% in males and 4.9% in females during 2015–16). Childhood obesity is more common in African-Americans, Hispanics, and American Indians when compared with Caucasians. In the 12–19 age group, African-American adolescent girls had the highest prevalence of obesity (28%), followed by Hispanic girls (20%) and Caucasian girls (15%). For boys the highest obesity was in Hispanics (22%), followed by African-Americans (19%) and Caucasians (17%).

In multiethnic 4-year-olds born in the United States, 18.4% were obese. The highest obesity prevalence was in American-Indian/Native Alaskan children (31.2%), followed by Hispanics (22%), African-Americans (20.8%), Caucasians (15.9%), and Asians (12.8%). Childhood obesity also varies by socioeconomic status. A national survey of preschoolers (2–4 years) revealed obesity to be 14.6% in low-income children than non-Hispanic Caucasian children (12.6%). The risk of become obese in adulthood is much higher when a child is overweight or obese. Elevated BMI continues from childhood to adulthood, even after taking into consideration parental obesity. The percentage of obesity in adults who were overweight as children is summarized in Table 1.3.

Focus on childhood obesity regarding education and income level

The prevalence of obesity is lower with a higher level of parental education, for children and adolescents aged 2–19 years. Obesity prevalence is lower in the highest income group among non-Hispanic Asian and Hispanic boys. Obesity prevalence is also lower in the highest income group among non-Hispanic Caucasian, non-Hispanic Asian, and Hispanic girls. Obesity prevalence did not differ by income among non-Hispanic African-American girls.

Table 1.3

Risk factors in early life and the development of later obesity

In studies of parents and their children, factors that impact adult obesity have been identified. These include diabetes mellitus, maternal obesity, malnutrition, and stressors during gestation, which include immunological, pharmacological, and psychological stressors. The child is more like to develop obesity, with potential long-term effects. Maternal weight, excessive weight gain during pregnancy, and infant birth weight are predictors of adult BMI after adjusting for normal childhood growth and development. Obesity in later life has been associated postnatally, with maternal diet and health, infant feeding patterns, and adiposity rebound.

Early adiposity rebound and future health risks

In early life, adipose tissue usually increases over the first year but decreases in the second year. It increases again between ages 3 and 8. The term adiposity rebound refers to an age at which BMI reverses direction at its lowest point and increases toward adiposity. Early onset of adiposity rebound, under age 5, is related to later-life obesity. This is independent of parental obesity and BMI when the rebound occurs. In one study of severely obese adolescents in France, 97% had experienced adiposity rebound at only age 2. Also, many children who had early adiposity rebound were of normal weight when it occurred.

Health consequences of childhood obesity

In children, health consequences of obesity affect multiple body systems, as in adults. There are higher risks for dyslipidemia, hypertension, hyperglycemia, hyperinsulinemia, and chronic inflammation. Obese children may also be at increased risk for asthma, obstructive sleep apnea, orthopedic problems, psychological distress, and psychosocial stigma. More than 50% of overweight children (5–10 years of age) are estimated to have one or more cardiovascular risk factors, such as dyslipidemia, hyperinsulinemia, or hypertension. While childhood obesity is linked to earlier onset of obesity-related adult diseases, incidence of adolescent type 2 diabetes has been shown to increase by 10 times.

Pathophysiology

Central or upper body fat distribution is a more accurate predictor of metabolic complications of obesity, compared to total body fat. Adipose tissue releases free fatty acids (FFAs) and glycerol into the bloodstream, via lipolysis. This provides 50%–100% of our daily energy requirements. Adipose tissue lipolysis is mostly inhibited by insulin and stimulated by catecholamines. However, growth hormone, cortisol, and atrial natriuretic peptide also stimulate lipolysis. Several abnormalities of adipose tissue lipolysis are associated with upper body obesity. Mostly, this is with higher postprandial FFA release and concentrations. The abnormality is especially evident in people with type 2 diabetes mellitus. Very high FFAs contribute to many metabolic complications.

Insulin resistance refers to insulin’s ability to promote glucose uptake and to inhibit glucose release into the bloodstream. Insulin-stimulated glucose uptake, oxidation, and storage mostly occur in the skeletal muscles. The liver is the main site of glucose production. Insulin resistance first leads to hyperinsulinemia, and eventually, to type 2 diabetes mellitus. With upper body obesity the ability of insulin to promote glucose uptake, oxidation, and muscle storage, and to suppress plasma FFAs, is reduced. High plasma FFAs can cause insulin resistance in muscles (glucose uptake) and in the liver (glucose release) that is independent of obesity. Therefore abnormal regulation of adipose tissue FFA export is important in insulin resistance development (see Chapter 4: Cardiovascular disease and its risk factors). Excess FFAs may cause muscle insulin resistance via increased synthesis of diacylglycerols and ceramides. These components both interfere with the normal pathway of insulin signaling. Dysregulated production of many adipokines, derived from adipose tissue, may contribute to insulin resistance and metabolic complications. Adiponectin is also derived from adipose tissue. It is a hormone that improves insulin action and is secreted in smaller rates in obesity and diabetes. In animal studies, insulin resistance has been linked to increased production of resistin, interleukin-6, tumor necrosis factor, and retinol-binding protein-4. Human studies are lacking, concerning the role of adipokines in metabolic complications of obesity.

Type 2 diabetes usually occurs when there are defects in insulin secretion and action. A large amount of obese patients are insulin resistant, but only some of them develop diabetes mellitus. Those with type 2 diabetes develop pancreatic beta-cell decompensation, followed by hyperglycemia. Animal studies suggest that lipotoxicity occurs when the beta cells fail. Increased FFAs may contribute to abnormalities of insulin secretion in obesity, leading to beta-cell failure. Elevated FFAs may have adverse effects upon islet beta-cell function in humans. The overproduction of islet amyloid polypeptide may be another contributing factor. This protein is secreted along with insulin. It has a tertiary structure, allowing it to form toxic amyloid deposits in the beta cells. Amyloid deposits have been seen in the pancreatic islets of autopsied patients who had diabetes mellitus type 2.

Type 2 diabetes and upper body obesity are related to increased triglycerides, decreased high-density lipoprotein (HDL) cholesterol, and a large proportion of small, dense, low-density lipoprotein (LDL) particles. This dyslipidemia increases cardiovascular risks seen in metabolic syndrome. There is fasting hypertriglyceridemia due to increased liver secretion of very low-density lipoprotein (VLDL), affected by increased FFAs reaching the liver from the visceral fat and upper body subcutaneous fat. Reduced HDL cholesterol concentrations and higher small, dense LDL particles related to upper body obesity are probably an indirect result of elevated triglyceride-rich VLDL. The atherogenic changes in triglycerides and cholesterol between lipoproteins may come from the increased cholesterol ester transfer protein activity and liver lipase activity. These lipid abnormalities are greatly influenced by genetics. Increased triglycerides and decreased HDL are all linked to polymorphisms in the genes for apolipoprotein E, apolipoprotein A-II, apolipoprotein B-100, and lipoprotein lipase.

Complications

The complications of obesity are very extensive and will be discussed in greater detail later in this book, based on chronic disorders of separate body systems. Many of the complications of obesity can reduce the quality of life and also shorten the lifespan. The consequences of obesity include the following:

• cardiovascular disorders

• diabetes mellitus

• certain cancers

• sleep apnea

• metabolic syndrome

• osteoarthritis

• tendon and fascial disorders

• gastroesophageal reflux

• liver disorders

• gallbladder disease

• reproductive system disorders

• urologic problems

• skin disorders

• social, economic, and psychological problems

It should be noted that metabolic syndrome, diabetes mellitus, and coronary artery disease are more likely in patients with fat that is concentrated abdominally, high serum triglyceride, family history or type 2 diabetes mellitus or premature cardiovascular disease, or combinations of these factors. Sleep apnea is an often-undiagnosed condition that causes loud snoring, excessive daytime sleepiness, and increased risks for hypertension, cardiac arrhythmias, and metabolic syndrome. The obesity-hypoventilation syndrome, also called Pickwickian syndrome, involves impaired breathing that causes hypercapnia, lowered sensitivity to carbon dioxide in stimulating respiration, hypoxia, cor pulmonale, and risk of premature death. This syndrome may occur alone, or secondary to sleep apnea. Being overweight or obese increases likelihood of developing gout, deep venous thrombosis, and pulmonary embolism. Obese people experience social, economical, and psychological problems because of others who treat them with prejudice, discrimination, poor body image, and lowered self-esteem. Extremely heavy individuals are sometimes underemployed or unemployed. Each of these topics will be discussed later.

Weight cycling

Weight cycling is commonly referred to as yo-yo dieting. It involves losing and then regaining weight multiple times. In the United States, between 10% and 40% of adult females have a history of weight cycling. The individual is able to successfully lose weight quickly but then regains it. Over time, these weight changes affect health, body fat distribution, body composition, and the expenditure of energy. Weight cycling is linked to higher risks for developing metabolic syndrome and coronary heart disease. All causes of mortality are increased with weight cycling, and even when a person’s BMI is in a health range, there is reduced quality of life. People who are obese but have extreme weight fluctuations have an increased taste preference for fat and sugar, making them likely to gain more weight in the future.

Diagnosis

The diagnosis of obesity is based on BMI, waist circumference, and in some cases, body composition analysis. To estimate an individual’s body fat percentage, health-care workers use a tool called a caliper to measure the thickness of a fold of skin (see Fig. 1.6). In adults, BMI is used to screen for being overweight or obese. A patient is considered overweight if his or her BMI is between 25 and 29.9 kg/m². Obesity is present if the BMI is 30 kg/m² or higher (refer back to Table 1.1).

Figure 1.6 Using a caliper to measure BMI in an obese person. BMI, Body mass index. Source: Photographed by the author.

Overall, BMI is a crude method of screening, since it does not take into account ethnicity, gender, or age. In some non-Caucasian people, for example, complications of obesity develop at a much lower BMI than in Caucasians. In children and adolescents, being overweight is defined as BMI at the 95th percentile or above. This is based on age-specific and gender-specific growth charts from the CDC. These charts are extensive and can be viewed at https://www.cdc.gov/growthcharts/clinical_charts.htm.

Other populations such as Asians have a lower cutoff of 23 kg/m² for being overweight. Also, BMI may be higher in muscular athletes, since they lack excess body fat. It may be normal or low in formerly overweight people who have lost muscle mass. Waist circumference along with present metabolic syndrome is better predictive factors for risks of metabolic and cardiovascular complications than BMI alone. Waist circumference that increases risks of complications due to obesity is varied as follows:

• Caucasian men: 93 cm (36.6 in.) or more, but especially when waist circumference is 101 cm (39.8 in.) or more

• Caucasian women: 79 cm (31.1 in.) or more, but especially when waist circumference is 87 cm (34.2 in.) or more

• Asian/Indian men: 78 cm (30.7 in.) or more, but especially when waist circumference is 90 cm (35.4 in.) or more

• Asian/Indian women: 72 cm (28.3 in.) or more, but especially when waist circumference is 80 cm (31.5 in.) or more

Body composition is the percentage of body fat and muscle. It is also considered when obesity is being diagnosed. While it may not be required in routine clinical practice, body composition analysis can be assistive if elevated BMI is because of muscle or excessive fat. Percentage of body fat is estimated by measuring skinfold thickness, usually over the triceps muscles, or by determining mid-upper arm muscle area.

Bioelectrical impedance analysis (BIA) estimates the percentage of body fat easily, without being invasive. The BIA estimates the percentage of total body water directly, and then the percentage of body fat is determined indirectly. This method is reliable in healthy patients, and in those who have a few chronic disorders that do not alter the percentage of total body water, such as diabetes mellitus or moderate obesity. It is uncertain whether the BIA method can be used for patients who have implanted defibrillators.

Hydrostatic weighing is the preferred, and most accurate, method for measuring percentage of body fat. However, it is costly and time-consuming and is primarily used in research studies, not clinical practice. For accurate weighing while submerged, the individual must fully exhale before the weighing process starts. In addition, in research studies only, percentage and distribution of body fat can be estimated via imaging procedures, which include computed tomography scan, magnetic resonance imaging, and dual-energy x-ray absorptiometry. It is important for obese patients to be screened for common comorbidities. These include obstructive sleep apnea, diabetes mellitus, dyslipidemia, fatty liver, depression, and hypertension.

Treatment

Obesity is considered to be a chronic disease that combines environmental, genetic, and behavioral factors. Treatment is also long-term. Though much weight can be lost by extreme calorie restriction, behavioral changes must occur to prevent regaining of weight—a common occurrence. Patients must learn how to make permanent changes in their eating and physical activity, in order to achieve permanent weight loss. Behavior modification helps patients recognize and avoid patterns of sedentary behavior and overeating. Intensive lifestyle intervention, and not simply education and support, results in less medications and hospitalization and lowered health-care costs for overweight or obese adults who have type 2 diabetes. The most efficient way to lose weight is to remove 500 kcal/day from the diet, resulting in about 1 lb lost per week. This is much easier to do than to increase energy expenditure by the same amount. However, higher levels of physical activity can prevent weight gain or regain after weight loss. Many patients need formal or informal behavioral modification changes in order to achieve their weight loss goals. Sometimes, pharmacotherapy or surgery is required. The treatment of obesity will be discussed in detail in Chapter 15, Obesity in the elderly.

Key terms

Alstrom syndrome

Atrial natriuretic peptide

Binge eating disorder

Bioelectrical impedance analysis

Ceramides

Craniopharyngioma

Cushing syndrome

Diacylglycerols

Dimorphic

Dual-energy x-ray absorptiometry

Fragile X syndrome

Genetic imprinting

Hunger-promoting hormones

Hydrostatic weighing

Hypercortisolism

Hyperinsulinism

Hyperplastic obesity

Hypertrophic obesity

Laurence–Moon–Biedl syndrome

Leptin

Lipolysis

Melanocortin

Melanocortin-4 receptor

Metabolic syndrome

Monogenic

Night-eating syndrome

Phenotypes

Pickwickian syndrome

Polygenic

Prader–Willi syndrome

Syndromic

Weight cycling

Further reading

1. Ahima RS. Obesity Epidemiology, Pathogenesis, and Treatment: A Multidisciplinary Approach Apple Academic Press 2014.

2. Akabas SR, Lederman SA, Moore BJ. Textbook of Obesity: Biological, Psychological and Cultural Influences Wiley-Blackwell 2012.

3. Bagchi D. Global Perspectives on Childhood Obesity: Current Status, Consequences and Prevention Academic Press 2010.

4. Bagchi D, Preuss HG. Obesity: Epidemiology, Pathophysiology, and Prevention 2nd ed. CRC Press 2012.

5. Blackstone RPP. Obesity: The Medical Practitioner’s Essential Guide Springer 2016.

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Chapter 2

Obesity and total mortality

Abstract

Today, the global pandemic of obesity is of utmost importance, created by a large increase in the amount of people who are overweight or obese over previous decades. Along with this increase, diabetes mellitus has similarly become more prevalent. Obesity is a strong predictor of type 2 diabetes and is linked to cardiovascular diseases, certain cancers, social stigma with resulting psychological problems, and disorders of the gastrointestinal, musculoskeletal, integumentary, respiratory, and reproductive systems. Childhood and adolescent cases of being overweight or obese are also increasing, resulting in diseases developing that were previously seen only in older people. Childhood obesity usually continues into adulthood, making it a lifelong problem. An economic cost of chronic obesity, on such a large scale, has the ability to overwhelm health-care systems and ruin the savings of families.

Keywords

Obesity; sedentary lifestyles; cardiovascular diseases; psychological problems; cancers; respiratory disorders; gastrointestinal disorders

Overview

Today, the global pandemic of obesity is of utmost importance, created by a large increase in the amount of people who are overweight or obese over previous decades. Along with this increase, diabetes mellitus has similarly become more prevalent. Obesity is a strong predictor of type 2 diabetes and is linked to cardiovascular diseases, certain cancers, social stigma with resulting psychological problems, and disorders of the gastrointestinal, musculoskeletal, integumentary, respiratory, and reproductive systems. Childhood and adolescent cases of being overweight or obese are also increasing, resulting in diseases developing that were previously seen only in older people. Childhood obesity usually continues into adulthood, making it a lifelong problem. An economic cost of chronic obesity, on such a large scale, has the ability to overwhelm health-care systems and ruin the savings of families.

Overall, though there are some fluctuations, obesity levels rise dramatically throughout the world, especially in poorer, developing countries that have more infectious diseases and hunger problems. Because of globalization and urbanization, physical activity levels of humans have generally become greatly reduced, along with changes in the diets of emerging countries. This causes a persistent positive energy balance, excessive weight gain, and obesity levels linked to increasing chronic diseases. The biggest obstacle against obesity is prevention.

Global prevalence of adult obesity

The World Health Organization (WHO), using surveys conducted since 2014, has created estimates of obesity prevalence in adults. These surveys use a body mass index (BMI) over 30 or more to define obesity. The global patterns of obesity prevalence for men are shown in Fig. 2.1, and for women, in Fig. 2.2. The range is lowest, at 5% of the populations of China, India, Japan, Korea, Pakistan, the Philippines, Vietnam, and several African countries. However, it is more than 60% of the populations of Polynesians living in the South Pacific. In developed countries, gender-specific estimates are two to three times higher than in developing nations. The prevalence of female obesity increases that of men by 5%–10% in most countries. In the United States the overall prevalence of obesity is about 41% in females and 38% in males.

Figure 2.1 Prevalence of obesity*, ages 18+, 2016 (age standardized estimate) male. Source: http://gamapserver.who.int/mapLibrary/Files/Maps/Global_Obesity_2016_Male.png.

Figure 2.2 Prevalence of obesity*, ages 18+, 2016 (age standardized estimate) female. Source: http://gamapserver.who.int/mapLibrary/Files/Maps/Global_Obesity_2016_Female.png.

Obesity develops because of an imbalance between consumed calories and expended calories. This is also known as energy input versus energy output. In nearly all-global areas the per capita dietary energy supply has greatly increased over the past 50 years. This mirrors the emergency of global obesity. For example, WHO estimates that the world daily per capita energy consumption increased, between 1960 and 2005, from 2250 to 2750 kcal. The link between the world patterns of energy consumption and the global patterns of male and female obesity illustrate the etiology between total calorie consumption and obesity.

Increased caloric intake with more cases of obesity and related diseases shows how populations throughout the world are eating more energy-dense foods that are high in fat and sugar. These foods are low in vitamins, minerals, and other micronutrients. The lack of physical activity because of more sedentary lifestyles, different types of available transportation, and increased urbanization all influence obesity and its negative outcomes. The top 10 countries with the highest average daily dietary energy consumption per capita, as of the years 2006–08, were as follows:

1. The United States—3800 kcal per day

2. Austria—3750 kcal

3. Greece—3710 kcal

4. Belgium—3690 kcal

5. Luxembourg—3680 kcal

6. Italy—3650 kcal

7. Malta—3600 kcal

8. Ireland—3590 kcal

9. Portugal—3580 kcal

10. Germany—3540 kcal

The 10 countries with the lowest average daily dietary energy consumption per capita in the same period, ranging between 1590 and 2020 kcal per day, were Eritrea, Burundi, Comoros, Haiti, Zambia, Ethiopia, Central African Republic, Angola, Chad, and Tanzania.

Prevalence of adult obesity in the United States

In the United States, obesity has tripled in prevalence in men, and more than doubled in prevalence in women since 1960. In that year, just 10% of men and 15% of women were obese. Table 2.1 shows the increases in male and female obesity between 1960 and 2015.

Table 2.1

In children and adolescents between 2 and 19 years of age, obesity prevalence increased from 13.9% in 2000 to 18.5% in 2015. The global prevalence of obesity is expected by the WHO to double between 2015 and 2030. For some reason, in the United States between 1999 and 2018, the obesity trend began to slow, according to the National Health and Nutrition Examination Survey (NHANES). However, this trend did not continue and obesity returned to a fast increase between 2015 and 2016. Current data suggests that approximately 70% of people ages 20 and older are either overweight or obese. Nearly 40% of them are now classified as obese.

Morbidity and mortality statistics

Increased morbidity, mortality, and poorer quality of life are all linked to obesity. According to WHO, there are 2.8 million deaths every year from being overweight or obese. This ranks these conditions in fifth place among the top 10 leading causes of death globally.

The formula used to calculate the disease burden of these conditions is as follows:

Based on calculations obtained from using this formula, being overweight or obese causes

• 44% of the disease burden from diabetes

• 23% of the disease burden from ischemic heart disease

• 7%–41% of the disease burden from many types of cancer

Obesity is definitely associated with premature death. Men who are obese at the age of 20 are twice as likely to die prematurely compared to nonobese men at the same age. At all ages, obesity continues to double the risk of early death up until 60 years of age. Also, for each BMI unit that is above normal, the risk of early death is increased by 10% throughout life. Obese men die about 8 years earlier than nonobese men.

In a Harvard University study of women aged 30–55, who did not have cardiovascular disease or cancer at the start of the 16-year-long follow-up, obese women had a 90% higher total mortality. This was more than four times higher for cardiovascular mortality, and more than twice as high for cancer mortality. The results showed that 53% of deaths among women with a BMI over 29 were because of their obesity. Also, gaining 10 kg or more of weight after age 18 and a BMI of more than 22 at age 18 predicted death from cardiovascular disease in middle adulthood. The lowest mortality rate was in thin women who maintained their weight since the age of 18.

The US National Institutes of Health evaluated BMI and all-cause mortality in men and women between the ages of 50 and 71. This study began in 1995 and had a follow-up of as much as 10 years. In people who never smoked and had no preexisting health conditions at the beginning, there was a regular increase of all-cause mortality as BMI levels rose from 26.5 to over 40, compared to a reference group who had BMI between 23.5 and 24.9. The men and women described as morbidly obese were more than twice as likely to die as those in the reference group. In a metaanalysis of 26 studies of men and women, from different racial and ethnic groups, over 60,000 died during follow-up out of a total of about 389,000. BMI categories and mortality were examined. Obesity-related heart disease mortality had a relative risk of 1.57; with cardiovascular disease, a risk of 1.48; and with cancer, a risk of 1.07. Total mortality was 22% in obese individuals compared to those of normal weight. Obesity leads to the onset of most chronic disease, via direct effects upon metabolic dysregulation. This appears clinically as hypertension, hyperinsulinemia, insulin resistance, dyslipidemia, hyperglycemia, and low-grade, chronic inflammation.

Gender differences in obesity

According to the NHANES between 2005 and 2006, the age-specific prevalence of obesity in men and women in the United States is different over the life span. Table 2.2 summarizes these differences.

Table 2.2

The difference between the genders regarding obesity is linked to the fact that women store excess fat needed for reproduction and lactation. There are many other factors, including variations in body composition, fat distribution, androgens and estrogens, eating behaviors and appetite, cultural and social differences, weight control and diet, patterns of exercise, basal metabolism, X and Y chromosomes and related genes, reproductive history, and menopause.

It is now understood that body fat distribution is heavily based on the differences in sex hormones. For example, in premenopausal women, estrogen may stop the oxidation of fatty acids, leading to increased body fat. This is especially prevalent at puberty and in early pregnancy. In women after menopause, adipose tissue in the abdominal and visceral areas increases, as ovarian estrogens are lost. In men, there is a slow decline in circulating androgens with aging. This results in accumulation of abdominal fat. Another factor is the administration of androgens, which has been shown to reverse abdominal obesity in men, but not in women. Estrogens appear to decrease visceral fat in aging people of both genders. Androgens decrease visceral fat in men but increase this fat in women.

Urban versus rural differences in obesity

In most countries, studies have shown that obesity is much more prevalent in urban areas than in rural areas. In China, which has very low obesity of approximately 2.9% of the population, some urban cities actually show prevalence of 20% or higher. Many African countries also have low obesity rates. However, research was done between 1992 and 2005 in seven African countries, showing that more wealthy people averaged 38% obesity, while poorer people averaged 21%. Obesity increased in the urban areas of these countries by 35%. However, the percentage increase in the poorest people, of 50%, was much higher than the increase in the richest people, of only 7%. Therefore obesity appears to be increasing in developing nations and may reach epidemic proportions, such as which have already occurred in developed nations.

Obesity has been a chronic problem in some areas of Africa, such as the Cape Peninsula of South Africa. In African women there, obesity levels since 1990 have been approximately 44%. Urban migration patterns in Africa have mirrored countries with emerging economies. The United Nations Population Division predicts that half of Africa’s population will live in urban areas by 2030. This is more than three times the amount or urban populations compared to 1950. This implies that the growing urbanization will impact the obesity epidemic.

Distribution of obesity by age, gender, and ethnicity in the United States

The distribution of obesity in the United States is different between various ages, genders, and ethnicities. In men, obesity is about 40% in young African-Americans and middle-aged Caucasians. In both genders of all ages, African-Americans have 44% obesity, while Hispanics have 39% and Caucasians have 33%. Obesity increases with age in African-American women, but not in other ethnicities (see Table 2.3). Prevalence is about 60% in African-American women who are age 60 and older. This is about double the levels of obesity in Caucasian and Hispanic women.

Table 2.3

Lifestyles of certain African-American women may predispose them to excessive weight gain and obesity. There is often a high intake of carbohydrates, fat, and sugar. Combined with high stress, physical inactivity, more pregnancies, low vitamin D, depression, lactose intolerance, and perceptions of body weight, outcomes are poorer for this group. Compared to other groups in weight management programs, studies reveal that African-American women are less likely to lose weight and maintain any weight loss.

Research and technology

The newest research concerning obesity and total mortality has revealed that in previous years, the link between them was underestimated. This is because prior studies relied on onetime measures of BMI, obscuring health impacts of weight change over time. The Proceedings of the National Academy of Sciences describes how earlier studies did not distinguish between people who never exceeded normal weight and people of normal weight who had been formerly been overweight or obese. The studies did not address the continuing effects of previous obesity and failed to account for the fact that weight loss is often related to an illness. Once these factors are taken into account, adverse health effects are more pronounced in weight categories that are above normal, and there is no protective effect of being overweight. It is now understood that the death rate for people who were normal weight at the time of the survey was 27% higher than the death rate for people whose weight never exceeded that category. There was a higher prevalence of both diabetes and cardiovascular disease in people who had reached excessive BMI and then lost weight, compared to people of people who remained in a high BMI category. Obesity at a particular age can predispose people to illness, regardless of subsequent loss of weight. For people in the normal-weight category at the time of the studies, 39% had transitioned into that category from higher weight