Body fat percentage, body mass index, skin thicknesses, and anthropomorphic measures

Obesity is a substantial public-health crisis in the United States and in the rest of the developed world. The prevalence is increasing rapidly in numerous developing nations worldwide. This growing rate represents a pandemic that needs urgent attention if its potential morbidity, mortality, and economic tolls are to be avoided.

The image below shows central nervous system neurocircuitry for satiety and feeding cycles.


Central nervous system neurocircuitry for satiety and feeding cycles.
The annual cost of managing obesity in the United States alone amounts to approximately $100 billion, of which approximately $52 billion are direct costs of healthcare. These costs amount to approximately 5.7% of all US health expenditure. The cost of lost productivity due to obesity is approximately $3.9 billion, and another $33 billion is spent annually on weight-loss products and services.

Body fat percentage, body mass index, skin thicknesses, and anthropomorphic measures

Obesity represents a state of excess storage of body fat. Although similar, the term overweight is puristically defined as an excess body weight for height. Although men have a body fat percentage of 15-20%, women have approximately 25-30%.^[1] Because differences in weight among individuals are only partly due to variations in body fat, body weight is a limited, though easily obtained, index of obesity.

The body mass index (BMI), also known as the Quetelet index, is used far more commonly than body fat percentage to define obesity. BMI is closely correlated with the degree of body fat in most settings. BMI = weight/height², where weight is in kilograms and height is in meters.

The body fat percentage can be estimated by using the Deurenberg equation, as follows: body fat percentage = 1.2(BMI) + 0.23(age) - 10.8(sex) - 5.4, where age is in years and sex is 1 for male and 0 for female. This equation has a standard error of 4% and accounts for approximately 80% of the variation in body fat.

Although the BMI is typically closely correlated with percentage body fat in a curvilinear fashion, some important caveats to its interpretation apply. In mesomorphic (muscular) persons, BMIs that usually indicate overweight or mild obesity may be spurious, whereas in some persons with sarcopenia (especially among persons of Asian descent), a typically normal BMI may conceal underlying excess adiposity characterized by increased percentage fat mass and reduced muscle mass.

In view of these limitations, some authorities advocate a definition of obesity based on percentage body fat. For men, percentage body fat greater than 25% defines obesity, and 21-25% is borderline. For women, over 33% defines obesity, and 31-33% is borderline.

Taller children generally tend to be more obese than shorter peers, are more insulin-resistant, and have increased leptin levels.^[2]

Other indices used to estimate the degree and distribution of obesity include the 4 standard skin thicknesses (ie, subscapular, triceps, biceps, suprailiac) and various anthropometric measures, of which waist and hip circumferences are the most important.

Although several classifications and definitions for degrees of obesity are accepted, the most widely accepted is the World Health Organization (WHO) criteria based on BMI. Under this convention for adults, grade 1 overweight (commonly and simply called overweight) is a BMI of 25-29.9 kg/m². Grade 2 overweight (commonly called obesity) is a BMI of 30-39.9 kg/m². Grade 3 overweight (commonly called severe or morbid obesity) is a BMI greater than or equal to 40 kg/m².

The surgical literature often uses a different classification to recognize particularly severe obesity. In this setting, a BMI greater than 40 kg/m² is described as severe obesity, a BMI of 40-50 kg/m² is termed morbid obesity, and a BMI greater than 50 kg/m² is termed super obese.

The definition of obesity in children involves BMIs greater than the 85th (commonly used to define overweight) or the 95th (commonly used to define obesity) percentile, respectively, for age-matched and sex-matched control subjects.

Apart from total body fat mass, accumulating data suggest that regional fat distribution substantially affects the incidence of comorbidities associated with obesity.^[3] High abdominal fat content (including visceral and, to a lesser extent, subcutaneous abdominal fat) is strongly correlated with worsened metabolic and clinical consequences of obesity. As a result, android obesity, which is predominantly abdominal, is more predictive of adipose-related comorbidities than gynecoid obesity, which has a relatively peripheral (gluteal) distribution. See image below.

A study by Losina et al explored the association of obesity and knee osteoarthritis.^[4] The study found that a substantial number of quality-adjusted life-years were lost due to knee osteoarthritis and obesity, most notably among black and Hispanic women.

An elevated BMI during adolescence (within the range currently considered normal) strongly associates with the risk of developing obesity-related disorders later in life.^[5] Although the BMI closer to onset of diabetes predicts risk of diabetes, elevated BMI both during adolescence and adulthood strongly predict the risk of CAD later in life. This observation lends support to the notion that process of atherogenesis CAD begins earlier than the manifestation of diabetes.

Obesity is associated with a host of potential comorbidities that significantly increase the potential morbidity and mortality associated with the condition. Although no cause-and-effect relationship is exhaustively demonstrated for all these comorbidities, amelioration of these conditions after substantial weight loss suggests that obesity probably plays an important role in their development.

Next Section: Pathophysiology

Pathophysiology

The pathogenesis of obesity is far more complex than the simple paradigm of an imbalance between energy intake and energy output. Although this concept allows easy conceptualization of the various mechanisms involved in the development of obesity, obesity is far more than the mere result of too much eating and/or too little exercise. However, the prevalence of inactivity in developed countries is considerable and relevant. In the United States, only approximately 22% of adults and 25% of adolescents report notable regular physical activity. Approximately 25% of adults in the United States report no remarkable physical activity during leisure, while approximately 14% of adolescents have similar reports of inactivity. See energy balance equation below.

Two major groups of factors with a balance that variably intertwines in the development of obesity are genetics, which is presumed to explain 40-70% of the variance in obesity, and environmental factors. Although the high prevalence of obesity in the children of parents who are obese and the high concordance of obesity in identical twins suggest a substantial genetic component to the pathogenesis of obesity, the secular trends of the last few decades, which have been coincident with changes in dietary habits and activity, also suggest an important role for environmental factors.

Friedman and colleagues discovered leptin (from the Greek word leptos, meaning thin) in 1994 and ushered in an explosion of research and a great increase in knowledge about regulation of the human feeding and satiation cycle. Since this discovery, neuromodulation of satiety and hunger with feeding has been found to be far more complex than the old, simplistic model of the ventromedial hypothalamic nucleus and limbic centers of satiety and the feeding centers of the lateral hypothalamus. Leptin is a 16-kD protein produced predominantly in white adipose tissue and, to a lesser extent, in the placenta, skeletal muscle, and stomach fundus in rats. Leptin has a myriad of functions in carbohydrate, bone, and reproductive metabolism that are still being unraveled, but its role in body weight regulation is the main reason it came to prominence.

The major role of leptin in body-weight regulation is to signal satiety to the hypothalamus and, thus, reduce dietary intake and fat storage while modulating energy expenditure and carbohydrate metabolism to prevent further weight gain. Unlike the Ob/Ob mouse model in which this peptide was first characterized, most humans who are obese are not leptin deficient but rather leptin resistant. Therefore, they have elevated circulating levels of leptin.

Lieb et al assayed plasma leptin in 818 elderly participants in the Framingham Heart Study.^[8] Leptin levels, which were higher in women, were strongly correlated with BMI. On follow-up (mean, 8 y), it was found that congestive heart failure had developed in 129 participants (out of 775 individuals who had been free of congestive heart failure), a first cardiovascular disease event had occurred in 187 participants (out of 532 individuals who had been free of cardiovascular disease), and 391 persons had died. The authors' data indicated that higher circulating leptin levels were associated with a greater risk of congestive heart failure and cardiovascular disease but that leptin did not offer incremental prognostic information beyond BMI.

Although more than 90% of human cases of obesity are polygenic, the recognition of monogenic variants has greatly enhanced our knowledge about the etiopathogenesis of obesity.^[9]

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The prevalence of obesity worldwide is increasing, particularly in the developed nations of the Northern hemisphere, such as the United States, Canada, and most countries of Europe. Available data from the Multinational Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) project suggest that at least 15% of men and 22% of women in Europe are obese.

Similar data now are being reported from many developing countries, particularly in those in Asia and, to a lesser extent, those in Africa. Reports from countries such as Malaysia, Japan, Australia, New Zealand, and China detail an epidemic of obesity in the past 2-3 decades. Data from the Middle Eastern countries of Bahrain, Saudi Arabia, Egypt, Jordan, Tunisia, and Lebanon, among others, indicate this same disturbing trend, with alarming levels of obesity often exceeding 40% and particularly worse in women than in men.

Data from the Caribbean and from South America also highlight similar trends. Although data from Africa on this issue are scant, a clear and distinct secular trend of profoundly increased BMIs is clearly observed when people from Africa immigrate to northwestern hemispheric countries. Comparisons of these indices among Nigerians and Ghanaians residing in their native countries with indices in recent immigrants to the United States show this trend poignantly.

Conservative estimates suggest that as many as 250 million people (approximately 7% of the estimated current world population) are obese. Two- to three-times more people than this are probably overweight. Although socioeconomic class and the prevalence of obesity are negatively correlated in most developed countries, including the United States, this correlation is distinctly reversed in many relatively undeveloped areas, including China, Malaysia, parts of South America, and sub-Saharan Africa.

Finucane et al conducted a comprehensive, constructive study that revealed growing global trends in BMI. This study may serve as wake-up call and initiate large-scale interventions in an effort to combat increasing body weight and associated adverse health consequences.^[12]

Some evidence suggests that, if unchecked, trends in obesity in the United States may be associated with overall reduced longevity of the population in the next few years. Data also show that obesity is associated with an increased risk and duration of lifetime disability. Furthermore, obesity in middle age is associated with poor indices of quality of life at old age.

The mortality data appear to have a U - or J -shaped conformation in relation to weight distribution.^[14] However, the degree of obesity (generally indicated by the BMI) at which mortality discernibly increases in African Americans and Hispanic Americans than in white Americans; this observation suggests a notable racial spectrum and difference in this effect. Underweight was associated with substantially high risk of death in a study of Asian populations. A high BMI is also associated with an increased risk of death, except in Indians and Bangladeshis.^[15]

The optimal BMI in terms of life expectancy is about 23-25 for whites and 23-30 for blacks. Emerging data suggest that the ideal BMI for Asians is substantially lower than that for Caucasians. For subjects with severe obesity (BMIs ≥40), life expectancy is reduced by as much as 20 years in men and by about 5 years in women. Coexisting obesity and smoking are associated with even greater risks than these for premature mortality.

A study by Berrington de Gonzalez et al confirms health advantages of normal BMI (20-24.9) and reinforces that both overweight and underweight have deleterious consequences—increased death risk.^[16]

Several factors modulate the morbidity and mortality associated with obesity. They include age of onset and duration of obesity, severity of obesity, amount of central adiposity, other comorbidities, sex, and level of cardiorespiratory fitness.

Obesity is a cosmopolitan disease that affects all races worldwide. However, certain ethnic and racial groups appear to be particularly predisposed. The Pima Indians of Arizona and other ethnic groups native to North America have a particularly high prevalence of obesity. In addition, Polynesians, Micronesians, Anurans, Maoris of the West and East Indies, African Americans in North America, and the Hispanic populations (both Mexican and Puerto Rican in origin) in North America also have particularly high predispositions to developing obesity.

Secular trends clearly emphasize the importance of environmental factors (particularly dietary issues) in the development of obesity. In many genetically similar cohorts of the high-risk ethnic and racial groups mentioned above, the prevalence for obesity in their countries of origin might be low, but this rate considerably changes when such groups emigrate to the affluent countries of the Northern hemisphere, where they alter their dietary and activity habits. These findings form the core concept of the thrifty gene hypothesis that Neal and colleagues espoused.

See also Mortality/Morbidity above.

No significant sex difference is reported in the prevalence of obesity.

The prevalence and age distribution of obesity has substantially changed in the last 2-3 decades.

Although the prevalence has remained at 30-50% of the adult population in the United States, the prevalence in children has increased to 15-25%.

As evidenced in secular trends, children and particularly adolescents who are obese have a high probability of growing to be adults who are obese; hence, the bimodal distribution of obesity portends a large-scale obesity epidemic in the next few decades.

Adolescent obesity poses a serious risk for severe obesity during early adulthood, particularly in non-Hispanic black women. This would call for stronger emphasis on reduction during early adolescence specifically targeting groups with greater risk.^[17]

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In most patients, the presentation is straightforward, with the patient indicating problems with weight or repeated failure in achieving sustained weight loss. However, in other cases, the subject may present with complications and/or associations of obesity.

A full history must include a dietary inventory and an analysis of the subject's activity level.

Screening questions to exclude depression are vital because this may be a consequence or a cause of excessive dietary intake and reduced activity.

Because almost 30% of patients who are obese have eating disorders, screen for these in the history. The possibility of binging, purging, lack of satiety, food-seeking behavior, and other abnormal feeding habits must be identified because management of these habits is crucial to the success of any weight-management program.

Also, determine if any of the previously mentioned comorbidities have occurred, and include questions to exclude the possible and rare secondary causes of obesity. See image below.

Comorbidities related to obesity include the following:

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  Cardiovascular - Essential hypertension, coronary artery disease,^[18] left ventricular hypertrophy, cor pulmonale, obesity-associated cardiomyopathy, accelerated atherosclerosis, pulmonary hypertension of obesity
  
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  CNS -Stroke, idiopathic intracranial hypertension, meralgia paresthetica
  
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  GI - Gall bladder disease (cholecystitis, cholelithiasis), nonalcoholic steatohepatitis (NASH), fatty liver infiltration, reflux esophagitis
  
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  Respiratory -Obstructive sleep apnea,^[19]obesity hypoventilation syndrome (Pickwickian syndrome), increased predisposition to respiratory infections, increased incidence of bronchial asthma
  
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  Malignant - Association with endometrial, prostate, gall bladder, breast, colon, and, possibly, lung cancer^[20]
  
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  Psychologic - Social stigmatization, depression
  
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  Orthopedic -Osteoarthritis, coxa vera, slipped capital femoral epiphyses, Blount disease and Legg-Calvé-Perthes disease, chronic lumbago
  
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  Metabolic -Insulin resistance, hyperinsulinemia, type 2 diabetes mellitus (see image below), dyslipidemia (characterized by high total cholesterol, high triglycerides, normal or elevated low-density lipoprotein, and low high-density lipoprotein)
  

Simplified scheme for the pathophysiology of type 2 diabetes mellitus.

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  Reproductive - Anovulation, early puberty, infertility, hyperandrogenism and polycystic ovaries in women, hypogonadotropic hypogonadism in men
  
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  Obstetric and perinatal -Pregnancy-related hypertension, fetal macrosomia, pelvic dystocia^[21]
  
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  Surgical - Increased surgical risk and postoperative complications, including wound infection, deep venous thrombosis, pulmonary embolism, and postoperative pneumonia
  
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  Pelvic - Stress incontinence
  
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  Cutaneous - Intertrigo (bacterial and/or fungal), acanthosis nigricans, hirsutism, increased risk for cellulitis and carbuncles
  
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  Extremity - Venous varicosities, lower extremity venous and/or lymphatic edema
  
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  Miscellaneous - Reduced mobility, difficulty maintaining personal hygiene
  

In the clinical examination, measure anthropometric parameters and perform the standard, detailed examination required in evaluating people with any chronic multisystemic disorder, such as obesity. Waist and hip circumference are useful surrogates in estimating visceral fat. Serial tracking of these measurements helps in estimating the clinical risk over time.

Neck circumference is predictive of a risk of sleep apnea, and its serial measurement in the individual patient is clinically useful for risk stratification.^[19]

In the skin examination, include a search for hirsutism in women, intertriginous rashes, acanthosis nigricans, and possible contact dermatoses.

A detailed cardiac and respiratory evaluation is crucial to exclude cardiomegaly and respiratory insufficiency.

In the abdominal examination, attempt to exclude tender hepatomegaly (which may suggest nonalcoholic steatohepatitis [NASH]) and distinguishing the striae distensae from the pink and broad striae that suggest cortisol excess.

When examining the extremities, search for joint deformities (eg, coxa vara), evidence of osteoarthrosis, and any pressure ulcerations.

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The etiology of obesity is multifactorial.

Among the facets to be considered in the development of obesity are the following:

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  Metabolic factors
  
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  Genetic factors
  
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  Level of activity
  
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  Behavior
  
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  Endocrine factors
  
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  Race, sex, and age factors
  
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  Ethnic and cultural factors
  
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  Socioeconomic status
  
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  Dietary habits
  
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  Smoking cessation
  
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  Pregnancy and menopause
  
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  Psychologic factors
  
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  History of gestational diabetes
  
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  Lactational history in mothers
  

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  Adiposa dolorosa (Dercum disease)
  
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  Partial lipodystrophies associated with localized lipohypertrophy
  

Various causes of anasarca may be mistaken as obesity if not carefully evaluated clinically.

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