Obesity

Chapter 36 Obesity



Gregory J. Anderson, Donald D. Hensrud



Chapter contents


Overview 802

Assessment 804

Demographics 805
Gender Differences 805

Race and Ethnic Origin 805

Socioeconomic Status 805

Education Level 805

Rural and Urban Differences 806

Age 806

Determinants of Obesity 806
Genetics vs. Lifestyle 806

Lifestyle Influences 807

Endocrine and Metabolic Factors 807

Medical Complications 808
Hypertension 808

Dyslipidemia 808

Type 2 Diabetes Mellitus 808

Metabolic Syndrome 809

Heart Disease 809

Cancer 809

Obstructive Sleep Apnea 809

Pulmonary Disease 809

Fatty Liver Disease 810

Orthopedic Disorders 810

Gallbladder Disease 810

Psychological Impact 810

Complications in Childhood and Adolescence 810

Management and Interventions 810
Childhood Overweight and Obesity 810

Management in Adults 811

Setting Goals 812

Diet 812

Physical Activity and Exercise 814

Behavioral Approaches 814

Medications 814

Complementary and Alternative Medicine 815

Surgery 815

Summary 817


Overview



Key Points


• Body mass index (BMI) determines the classification of obesity for clinical use.

• Waist circumference reflects the distribution of adipose tissue and helps determine obesity risk.

• Central obesity, reflected by a high waist measurement, is associated with more complications.

Obesity has been a rapidly developing health concern in the United States. The ongoing Behavioral Risk Factor Surveillance System (BRFSS) and National Health and Nutrition Examination Survey (NHANES) provide a longitudinal view of changes in the obesity problem. BRFSS data are from a state-based telephone survey, and NHANES data are based on measurements of a representative sample of the U.S. population. The self-reporting design of BRFSS tends to underestimate weight, but ongoing studies can be examined for trends. NHANES reported that the prevalence of U.S. adults in the overweight category (BMI ≥25 kg/m2) increased from 46% to 61% between the late 1970s and 1990s (Zimmerman, 2002). As of 1999–2000, 64.5% of adults were overweight and 30.5% were obese (BMI ≥30 kg/m2) (Flegal et al., 2002). Prevalence estimates from the Centers for Disease Control and Prevention (CDC) for 2007–2008 found that 32.2% of men and 35.5% of women were obese. In addition, surveys from 1976–1980 and 2003–2006 found that obesity increased from 5.0% to 12.4% among children age 2 to 5 years; from 6.5% to 17.0% for ages 6 to 11 years; and 5.0% to 17.6% for ages 12 to 19 years. Changes in obesity prevalence have affected all U.S. regions (Fig. 36-1).


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Figure 36-1 U.S. maps reflecting changes in obesity prevalence estimates over time.


(Courtesy Centers for Disease Control and Prevention. Behavioral Risk Factor Surveillance System.)


The problem of obesity is not limited to the United States. Globally, overnutrition has now surpassed undernutrition as a public health concern. An estimated 8.5% of the world population is overweight versus 5.8% underweight (Zimmerman, 2002). Although obesity prevalence estimates vary among countries, the World Health Organization (WHO) has projected that 2.3 billion adults will be overweight and 700,000 million obese by 2015.


Improved treatment of comorbidities has made assessing obesity’s impact on mortality more difficult, but estimates of the excess mortality associated with obesity in the United States range from 100,000 to 300,000 deaths each year. Persons in the overweight category have 20% to 40% increased mortality, and obese persons have a twofold to threefold increase in mortality (Adams et al., 2006).


The increased prevalence of obesity has many other health ramifications. An increase in body mass index (BMI) is a risk factor for short-term disability in the workplace. Overweight and obese individuals have odds ratios of 1.26 and 1.76, respectively, compared to normal-weight workers (Arena et al., 2006). Obesity increases “presenteeism,” or the reduced productivity in workers still on the job. Workers with BMI over 35 kg/m2 experienced a 4.2% health-related drop in productivity (Gates et al., 2008). Evidence indicates that the 37% increase in obesity rates (BRFSS) between 1998 and 2006 is a significant factor driving health care costs. The medical consequences of obesity have been estimated to account for 9.1% of annual medical spending (Finkelstein et al., 2009).



Assessment


The primary parameter used to categorize weight is BMI: 18.5 and 24.9 is normal in adults; 25 to 29.9 is overweight; and 30 or greater is obese. Class III, “severe,” or “extreme” obesity is 40 and higher. Calculated from height and weight and expressed in kg/m2, BMI is a readily available tool in the assessment of obesity (Table 36-1). Because it correlates with total body fat and with the complications of obesity better than body weight, BMI is a recommended parameter to assess obesity, but an imperfect tool to measure adiposity. A high value may reflect greater lean body mass rather than adiposity in muscular individuals. In addition, BMI does not reflect distribution of body fat, a factor that influences risk.



Table 36-1 Obesity and Body Mass Index (BMI): Height and Weight

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Body fat percentage is a more precise assessment of adiposity but is difficult to measure accurately in the office setting. The techniques of skin fold measurements and bioelectric impedance assays can be used, but skin fold measurements may not be accurate, and both measures generally do not change assessment or treatment goals for most patients. Cutoff levels for body fat percentage selected by WHO are used to stratify health risks associated with overweight and obesity but may not be practical in clinical practice.


From birth to age 2 years, overweight is assessed by the weight-for-length percentile; at or above the 95th percentile is considered overweight or obese. For the pediatric population age 2 to 19 years, percentile ranks based on the 2000 CDC growth charts for the United States are used to define overweight and obesity. The CDC defines overweight between ages 2 and 19 years as a BMI between the 85th and 95th percentiles for age and sex. A child or adolescent with BMI at or above the 95th percentile is considered obese.


The distribution of body fat also affects health risks. Central obesity, also referred to as visceral, abdominal, or android obesity, is associated with a greater risk of complications, including the metabolic syndrome, as discussed later. Waist-to-hip ratio has been used to assess central obesity, but gender-specific waist circumference, taken at the level of the iliac crest, has proved to be a better assessment of the distribution of body fat. Health risks increase above a waist circumference of 35 inches in women and 40 inches in men, and as a continuous variable with increasing waist circumference, but these cutoffs facilitate a simple classification of risk in a continuous variable. Magnetic resonance imaging (MRI) and computed tomography (CT) of the abdomen have also been used to assess visceral deposition of fat in research settings, but cost and lack of easy accessibility make them impractical for clinical use. Table 36-2 lists the classification of obesity based on BMI and waist circumference.



Table 36-2 Classification of Obesity Based on BMI and Waist Circumference

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Demographics



Key Points


• Men are more likely than women to have central obesity.

• African Americans, Hispanics, and Native Americans are at greater risk of obesity than whites.

• Obesity is inversely related to education and socioeconomic status.

• Obesity is more prevalent in rural than urban areas.

Obesity is a concern within virtually all demographic groups (Table 36-3). The high prevalence of obesity is seen in both genders, most ethnic groups, and at all ages. Within those groups, the impact is not uniform.



Table 36-3 Obesity Prevalence (BRFSS Surveys, 2006–2008)

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Gender Differences


Men are more likely than women to be overweight, whereas women are more likely to be obese. Men, however, are more likely to have central obesity, associated with greater health risks.



Race and Ethnic Origin


African Americans, Hispanics, and Native Americans are at greater risk for obesity. Blacks have a 51% higher prevalence of obesity and Hispanics a 21% higher prevalence than whites (Pan et al., 2009). Asians are at lower risk as an ethnic group. However, health risks of overweight and obesity may appear at a lower weight in Asians, and thus a lower cutoff for overweight has been proposed for Asians (BMI >23 kg/m2). Gender differences are seen within ethnic groups. The prevalence of obesity is greater among African American women than among African American men, whereas these differences are not as evident among non-Hispanic whites. Immigrants have an increased incidence of obesity, starting about 10 years after arrival in the United States (Goel et al., 2004).



Socioeconomic Status


The increase in the prevalence of obesity worldwide reflects, in part, economic development. The prevalence ranges from approximately 2% in the least developed countries to over 30% in the most developed countries. In developed countries, however, lower socioeconomic status is associated with an increased risk. Proposed reasons for this observed difference include reduced access to medical care, healthy foods, and exercise facilities among lower socioeconomic groups. Furthermore, foods that are more energy dense (through the addition of added sugar) are less costly than nutrient-dense foods (Thompson et al., 2009).



Education Level


Education level is inversely related to the risk of obesity, which may partly explain the decreased risk with increased socioeconomic status in developed countries. Access to health care, greater awareness of healthy lifestyle habits, and more access to recreational facilities are potential factors in this association.



Rural and Urban Differences


Analysis of BRFSS data shows that the prevalence of obesity is greater in rural than urban areas. Factors that reduce physical activity may play a role, ranging from less access to exercise facilities to lack of sidewalks. Reduced availability of healthy food choices is also thought to contribute. As in other settings, African Americans and Native Americans in rural areas have the highest prevalence of obesity. Although Asians in urban environments have a low prevalence of obesity, the prevalence among Asians in rural settings approaches that of other ethnic groups (Jackson et al., 2005).



Age


The incidence of overweight increases steadily after age 20 until the seventh decade of life. At that point, it levels off and begins a gradual decline. Even within the low-risk age ranges of 18 to 29 and older than 70 years, the prevalence of overweight has increased according to BRFSS. The increased prevalence of overweight is especially alarming in the pediatric population, in whom the most dramatic increase has been in the severely obese, similar to the adult population. More than 30% of children and adolescents are overweight or obese. Older children are more likely to be in a higher weight category.



Determinants of Obesity



Key Points


• Obesity results from the interaction of genetic makeup, environment, and lifestyle.

• Genetic factors are estimated to account for 30% to 40% of the variability in adult weight.

• Genetic influence is polygenic.

• Specific metabolic or endocrine disorders account for less than 1% of the obese population.

When reduced to basics, obesity results from calorie consumption in excess of expenditure. What complicates this simple principle is the role of genetics, lifestyle, and environmental factors. Throughout human evolution there has been a survival advantage to storing energy as fat. The conveniences of modern life have led to a decrease in energy expenditure. At the same time, greater access to energy-dense food, along with other factors, has increased energy consumption. These changes, in the relatively recent past, negate the survival advantage of fat storage for most segments of the population.



Genetics vs. Lifestyle


The relative contribution of genes versus lifestyle and environment in the development of obesity has not been precisely delineated. A child’s risk of adulthood obesity is three times greater if one parent is obese and 10 times greater if both are obese. Indeed, for children younger than 3 years, parental weight is a greater determinant of risk of obesity than the child’s own weight (Whitaker et al., 1997). However, the influence of parental weight does not reflect only genetic predisposition, because family members also share the same environment. A correlation in adult weight between identical twins is seen, even when they have been raised apart. Among adoptees, weight correlates with the weight of their biologic parents, but the correlation is not as strong as in twin studies. In summary, genetic makeup plays a permissive role, with adult weight being determined by interaction with the environment. Overall, genetic factors are estimated to be responsible for 30% to 40% of the variability in adult weight.



Genetic Factors


Most of the genetic influence on obesity is polygenic. More than 250 genes and chromosomal regions are associated with phenotypic obesity (Larsen et al., 2003). In some cases, the genes code specifically for visceral as opposed to subcutaneous obesity. Although specific genetic factors to explain common obesity have not been identified, several single-gene defects cause obesity in animals, with some correlates in humans.


Single-gene mutations related to obesity often involve leptin and melanocortin. Leptin is a protein produced in adipose tissue that provides negative feedback to appetite control centers. Obesity may reflect lack of hormone production or a lack of leptin receptors. There are leptin-deficient animal models, and rarely, this deficiency has been identified in humans. In leptin-deficient people, weight loss results when leptin is replaced. Leptin supplementation in non–leptin-deficient obese subjects does not result in weight loss (Bray, 2002).


Rare defects in melanocortin receptors in the adrenals have also been associated with obesity. Most often, a person must be homozygous for the abnormal gene for the trait to be expressed. A defect in the melanocortin-4 receptor is the most common single-gene mutation associated with severe obesity but still accounts for only about 5% of this population. Other single-gene mutations have been found in animal models as well as humans, but all are extremely rare. Recently identified genes include the FTO (fat mass and obesity-associated) gene. Each of these genes seems to be associated with a modest increase in weight.


There are a number of congenital syndromes in which obesity is part of the phenotype. The best known, Prader-Willi syndrome, results from a defect in the long arm of chromosome 15 and causes poor muscle tone in the newborn period, with hyperphagia, hypogonadism, behavioral problems, and developmental delay noted later. As with other medical causes of childhood obesity, linear growth is poor while growth in weight is excessive. Although the exact mechanisms by which the genetic abnormalities lead to obesity are unclear, patients with Prader-Willi syndrome have elevated levels of ghrelin, a peptide produced in the stomach and duodenum that stimulates eating.



Modulation of Appetite


Many hormonal factors are involved in appetite, as well as in the absorption, storage, and use of calories. Factors providing input to the brain include leptin levels, vagal afferent activity, and fluctuation in plasma glucose levels. Neuropeptides and monoamine neurotransmitters are also involved in appetite control. Some weight loss medications exert their influence through modulation of neurotransmitter levels, which may affect appetite or satiety.



Influences on Central Obesity


Central obesity suggests increased visceral fat deposits, likely caused by increased production of peptides and other metabolic messengers. Hormonal influences most likely play a role in the distribution of fat. Central obesity is believed to result partly from increased androgenic effects, which is why men have a greater tendency for central obesity. Central obesity is also associated with hyperandrogenic states in women, such as polycystic ovary syndrome (PCOS). The increase in visceral deposition of fat that can occur after menopause in women may be related to a decrease in growth hormone and estrogen production (see Chapter 35).



Lifestyle Influences



Key Points


• Increased caloric intake is related in part to “portion distortion,” linked to eating away from home.

• Smoking cessation is associated with weight gain of 4 to 5 kg (on average).

• Many antidepressants, neuroleptics, and anticonvulsants are associated with weight gain.

• Decreased overall physical activity (not just “exercise”) is a major factor associated with the increasing prevalence of overweight and obesity.

As mentioned, obesity develops when caloric intake exceeds caloric expenditure against a background of genetic influences. The chief determinants of energy imbalance are lifestyle factors. Individual total energy requirements depend on the basal metabolic rate (BMR), thermic effect of food, and energy needed for the day’s physical activities. The chief determinant of BMR is the amount of lean body mass, which can be difficult to increase. Some data indicate that the thermic effect of food (amount of energy needed to absorb, digest, and assimilate nutrients) is lower in obese persons than in lean subjects, but this difference is quite small. Physical activity (exercise and activity throughout the day) is the most variable component of energy expenditure. The major reasons for weight gain are therefore excessive calorie intake and decreased overall physical activity.



Caloric Intake


Over the past 40 years, the tendency in the U.S. population has been to consume more calories needed; per-capita consumption of calories increased from 2220 kcal in 1970 to 2680 kcal in 1997 (Putnam, 2000). Some of this increase is related to increased portion size; a normal portion in 1970 is much less than a normal portion in 2010. This “portion distortion” has been linked to people eating more away from home. The typically larger restaurant portion size has been adopted as the in-home standard as well (Foreyt and Poston, 2002).


Energy density also plays a role. Satiety helps determine food intake and is largely determined by the volume and weight of food consumed. Foods that are high in caloric content for a given volume lead to excessive calorie intake. This includes fat and highly processed foods such as sugar and other refined carbohydrates that are high in energy density. Per-capita consumption of sugar has greatly increased at the same time as the increasing prevalence of obesity.


The frequency of meals may play a small role. Eating smaller meals more frequently is associated with less overweight. Large meals are associated with more insulin release. This might be a mechanism whereby meal size influences weight gain.



Activity Changes


Decreased energy expenditure may play a greater role in the development of obesity than increased caloric intake. In the United States a progressive decrease in energy expenditure has coincided with the increase in calorie consumption (Foreyt and Poston, 2002). The amount of exercise has not changed much over the past few decades, so most of the decrease in physical activity energy expenditure has occurred in daily physical activities, not exercise.



Smoking Cessation


Often cited by smokers as a reason to continue smoking, stopping cigarette smoking does lead to weight gain. The average weight gain is 4 to 5 kg (~9-11 lb) over months (Flegal et al., 1995). Typically, the person gains 1 to 2 kg (~2-4 lb) in the first few weeks after cessation (Bray, 2002). Approximately 10% of people gain 10 kg (22 lb) or more.



Medications


A number of medications are associated with weight gain, including antidepressants, antipsychotics, anticonvulsants, and hypoglycemic agents. Tricyclic antidepressants, monoamine oxidase inhibitors, and mirtazapine are the antidepressants most likely to cause weight gain. Of the more common selective serotonin reuptake inhibitors (SSRIs), paroxetine is most likely to be associated with weight gain, although individual effects vary. Many neuroleptics can lead to weight gain. Phenothiazines and haloperidol, as well as some newer agents such as clozapine and olanzapine, tend to increase weight. Among anticonvulsants, valproic acid and gabapentin have been most closely tied to weight gain. Lamotrigine is thought to be weight neutral, whereas topiramate may actually promote weight loss. Insulin, as well as oral hypoglycemics that increase production or release of insulin, promote weight gain. It should be noted that metformin, which increases insulin sensitivity, is associated with modest weight loss and may ameliorate the weight gain from other hypoglycemics. Chronic systemic steroid use can cause a cushingoid type of obesity.



Endocrine and Metabolic Factors


Specific identifiable endocrine or metabolic disorders known to cause obesity account for less than 1% of the obese population, contrary to what is commonly believed (see also Chapter 34).



Hypothyroidism


Although rarely found in children, hypothyroidism is associated with slow statural growth and developmental delay. More common among adults and more often seen in women, hypothyroidism is a relatively rare cause of obesity. If undiagnosed, it is typically accompanied by other symptoms of thyroid deficiency, such as cold intolerance, decreased energy, obstipation, and increased thinning of the scalp.



Neuroendocrine Factors


The rarely seen neuroendocrine causes for obesity result from injury to the ventromedial hypothalamus, the result of tumor, trauma, or surgery to the posterior fossa. Other symptoms indicative of endocrine and neurologic abnormalities are seen along with hyperphagia and subsequent obesity (Bray, 2002).



Cushing’s Syndrome


This endocrine disorder is associated with central obesity and “buffalo hump” along with axillary striae, glucose intolerance and hypertension. In children with Cushing’s syndrome, linear growth is restricted.



Polycystic Ovary Syndrome


More than 50% of women affected by this relatively common disorder are obese. Some controversy surrounds whether PCOS is a cause or consequence of obesity, although most evidence points to the latter. Other common features include menstrual irregularities, hirsutism, and elevated testosterone and luteinizing hormone blood levels. Insulin resistance is a consistent finding, even in the absence of obesity. This resistance is thought to be associated with other findings in PCOS, although exact mechanisms are unclear.



Growth Hormone Deficiency


Although growth in height is impaired in growth hormone deficiency, there is also an increase in truncal obesity. This corrects with replacement of growth hormone.



Medical Complications



Key Points


• Obesity is more closely related to elevated triglycerides and low HDL cholesterol than elevated total and LDL cholesterol.

• Weight loss is the most effective lifestyle change to lower blood pressure.

• Up to 80% of cases of type 2 diabetes mellitus are attributable to overweight and obesity.

• Obesity plays a role in 14% of cancer deaths in men and 20% in women.

Based on observational studies, obesity is a risk factor for a number of chronic medical conditions. In conjunction with other risk factors, obesity can greatly impact the chances of developing many diseases. In general, the increased risk for morbidity and mortality begins in the overweight range and correlates more strongly with BMI over 30 kg/m2 (Flegal et al., 2004). The risk of specific conditions associated with obesity, such as diabetes and hypertension, varies with gender and ethnic origin.



Hypertension


Obesity has long been recognized as a risk factor for hypertension and appears to be associated with the increasing incidence of hypertension seen with aging. The obesity-related increase in blood pressure (BP) is associated with an increase in vascular resistance as well as sodium resorption. The increased vascular tone may reflect increased sympathetic tone because of insulin resistance and the resultant increase in insulin levels. In the Nurses’ Health Study (NHS), for BMI at age 18 and again at midlife, the relative risk of hypertension in women gaining 5 to 9.9 kg (11-22 lb) in that time was 1.7, and in those with weight gain over 25 kg (55 lb) was 5.2 (Huang et al., 1998). Controlling overweight would reduce the incidence of hypertension in whites by an estimated 48% and in African Americans by 28% (Bray, 2003). Weight loss is the most effective lifestyle change to decrease blood pressure. For every 1-kg loss in weight, there is an average decrease of 0.6 mm Hg in systolic and 0.34 mm Hg in diastolic BP (Stevens et al., 1993). In the National Heart, Lung, and Blood Institute (NHLBI) obesity guidelines, weight loss is recommended to lower elevated BP in overweight and obese persons.



KEY TREATMENT



Modest weight loss can reduce morbidity of obesity-related disease (Shepherd, 2003) (SOR: A).


Dyslipidemia


Obesity is associated with elevated triglyceride (TG) levels, reduced high-density lipoprotein cholesterol (HDL-C), and an increase in the more atherogenic, small, dense LDL particles. Despite common belief, obesity causes only a small mean elevation in total and low-density lipoprotein cholesterol (LDL-C) values. There is strong evidence that weight loss through lifestyle measures will reduce TG and increase HDL-C levels. This weight loss is generally accompanied by a decrease in total cholesterol and LDL-C, in part because the same lifestyle changes in diet that decrease weight also decrease LDL-C. The favorable effect on lipids from aerobic exercise is most noticeable when accompanied by weight loss. NHLBI recommends weight loss to reduce elevated total cholesterol, LDL-C, and TG levels and to raise HDL-C in overweight/obese persons.



Type 2 Diabetes Mellitus


According to BRFSS, the prevalence of type 2 diabetes mellitus (T2DM) increased from 4.9% in 1990 to 7.9% in 2000 (Mokdad et al., 2003). This change has been clearly linked to the increase in obesity. The risk of T2DM is lowest below a BMI of 22 to 23 kg/m2. At a BMI of 31, the risk for women in the NHS was 40-fold greater than in women with a BMI less than 22 (Colditz et al., 1995). For men in the Health Professionals Follow-up Study, the risk of T2DM above a BMI of 35 kg/m2 was increased 60-fold. Up to 80% of cases of T2DM can be attributed to overweight and obesity. There appears to be a time delay of about 10 years between the development of overweight and onset of the diabetes (Bray, 2003). As weight increases, insulin resistance and compensatory insulin secretion also increase. At some point, the body’s ability to secrete insulin does not meet requirements, and blood glucose rises. Weight loss is recommended to lower elevated glucose levels in overweight and obese persons with T2DM.

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Oct 3, 2016 | Posted by in MANUAL THERAPIST | Comments Off on Obesity

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