Caballero B. (ed.) Encyclopaedia of Food Science, Food Technology and Nutrition. Ten-Volume Set

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work-related physical activity and energy expended

in activities of daily living has declined in the past few

decades. In the USA, however, leisure-time physical

activity has not changed much since 1985, with 60%

of the adults reporting that they are not regularly

active, and 25% reporting that they are not active

at all.

0039 The amount of energy required for daily living has

also decreased, owing to an increase in sedentary

activities such as watching television, VCR, remote

control, computer interactions, listening to music,

etc.

0040 Data from the national personal transportation

survey in the USA have shown that the number of

annual walking trips has declined significantly,

whereas the number of daily car trips has increased

by nearly an identical amount.

0041 Decreases in TDEE as a consequence of the above

factors would lead to obesity if energy intake were

not reduced to match the new level of energy expend-

iture, which seems to be happening in developed

countries. Even additional bouts of exercise, if

followed by a high-fat and high-energy diet, can to-

tally negate the energy expenditure of the exercise.

0042 An individual’s predisposition to engage in physical

activity may be influenced by their genotype. Vari-

ations in muscle metabolic characteristics, like oxida-

tive capacity, may play a role in the pathogenesis of

obesity. The increased proportion of fast-twitch (type

II B) as opposed to slow (type 1) muscle fibers in

obese individuals may be responsible for decreased

exercise tolerance and increased perception of fatigue

by some of these individuals, predisposing them to be

less active and gain weight.

Social and Cultural Factors

0043 Social and cultural factors also make important

contributions to the pathogenesis of obesity. The

range of BMI of a population varies significantly

according to the stage of transition to market econ-

omy and associated industrialization of a country,

urbanization, changing social structures, and socio-

economic status. In the initial stages of the transition,

the wealthier sections of society show an increase in

the proportion of people with a high BMI, whereas

in the later phases of transition, a high BMI among

the poor shows increasing prevalence. This is usually

accompanied by an increase in childhood and adoles-

cent obesity and obesity-related disorders.

0044 Cultural factors like cuisine, entertaining, and food

selection, fat content of diet, attitude toward health,

energy intake, body image, and physical activity also

play a role in influencing the range of BMI in a

population.

Fetal Undernutrition

0045Maternal malnutrition causing undernutrition of the

fetus during intrauterine development may determine

the later onset of obesity, independent of genetic

factors. In support of the hypothesis is the finding of

an inverse relationship between birthweight and adult

obesity, blood pressure, and type 2 diabetes, in both

men and women, in later life, with the highest BMI,

glucose concentrations, and systolic blood pressures

being observed in those with the lowest birthweight.

The mechanism of this is unclear.

Diagnosis

0046The diagnosis of obesity is generally not difficult,

but is is important to both quantify its degree and

determine the relative risk of complications based

on body-fat distribution, and other risk modifiers

such as personal or family history of complicating

conditions.

Body Mass Index

0047The body mass index (BMI) is accepted as the

standard measure of relative body weight, i.e., weight

adjusted for height. The BMI was found to correlate

significantly with total fat content in the body. It can

be used to assess overweight and obesity and to moni-

tor changes in body weight and determine the efficacy

of a treatment program.

0048BMI is calculated as weight in kilograms divided by

height in meters squared.

BMI ¼ weightðkgÞ=heightðmÞ

0049The formula using nonmetric measurements is

BMI ¼ 703 ðweight ðlb:Þ=height ðinÞ

Þ:

These values are independent of age and sex. Calcu-

lating BMI is simple, rapid, and inexpensive, and can

be applied generally to adults. Although there are a

number of accurate methods by which to assess body

fat (e.g., total body water, total body potassium,

bioelectrical impedance, and dual-energy X-ray

absorptiometry), the measurement of BMI is the

most practical approach in a clinical setting. This is

especially true because no trial data exist to indicate

that one measure of fatness is better than any other

for monitoring overweight and obese patients during

treatment.

0050Based on BMI, a standard classification of the

degree of overweight and obesity has been established

(Table 1). A BMI of > 25 confers increased risk for

a number of health conditions. There is strong evi-

dence that weight loss in overweight and obese indi-

viduals reduces risk factors for diabetes, coronary

4224 OBESITY/Etiology and Diagnosis

artery disease, strokes etc. While the risk of medical

complications generally increases with obesity class,

an important modifier is the distribution of excess

adipose tissue, as estimated most conveniently by

the waist circumference.

Waist Circumference

0051 Body fat may be preferentially located in the abdo-

men (android obesity pattern) or surrounding the hips

and thighs (gynoid obesity pattern). The android pat-

tern often reflects an accumulation of fat surrounding

the abdominal visceral organs. The presence of excess

fat in the abdomen out of proportion to total body fat

is an independent predictor of morbidity. Waist cir-

cumference is a clinically acceptable measurement for

assessing an individual’s abdominal fat content, and

they positively correlate with each other. The sex-

specific cut-off associated with increased relative

risk for the development of obesity-associated risk

factors, when the BMI is 24.9–34.9, is shown in

Table 2. When the BMI is more than 35, the waist

circumference is usually more than the cut-off and

thus does not have any additional predictive value.

The waist circumference is a better marker of abdom-

inal fat content than the waist-to-hip ratio and is the

most practical anthropometric measurement for esti-

mating a patient’s abdominal fat content before and

during weight-loss treatment.

Weight-for-Height Tables

0052 Historically, weight-for-height tables like the Metro-

politan Life Insurance Company table were used to

define the normal weight range. However, such tables

have major limitations, such as a reliance on primar-

ily white reference populations, use of unvalidated

estimates of frame size, and derivation of the table

from insurance company mortality data.

Assessment of Risk Status

0053 Adults with a BMI of 30 or more have a 1.5–2.0 times

relative risk of death from all causes compared with

individuals with a BMI of 20–25, with most of the

increase being due to cardiovascular causes. It is

therefore reasonable to assess an individual’s absolute

risk status by looking for the presence of the

following conditions:

0054Coronary heart disease Obesity is associated with

coronary heart disease (CHD), primarily via its impact

on the CHD risk factors of hypertension, dyslipid-

emia, and type 2 diabetes mellitus. Obesity may

also directly confer some increased risk of coronary

artery disease (CAD) though. Besides BMI, exces-

sive abdominal fat has also been shown to have a

positive correlation with morbidity and mortality

from CAD. Body weight, independent of risk

factors, is also directly related to the development

of left ventricular hypertrophy and congestive car-

diac failure, perhaps via increased cardiac work-

load, and changes in vascular resistance and blood

return. Obese individuals should also be evaluated

for other cardiovascular risk factors, especially

smoking and family history of CAD, as these may

magnify the obesity-associated risk.

0055Type 2 diabetes mellitus Excess body fat is associ-

ated with increased insulin resistance and risk of

developing type 2 diabetes mellitus. This correlation

is strengthened by the fact that a significant majority

of people with type 2 diabetes mellitus are obese.

Moreover, the dramatic increase in obesity during

the past decade has been accompanied by a dramatic

increase in the prevalence of type 2 diabetes mellitus.

In fact, overweight and obesity, especially in those

with a more central body fat distribution, are the

major risk factors for the development of type 2

diabetes mellitus.

0056Obstructive sleep apnea Obstructive sleep apnea

syndrome (OSA) is characterized by occlusion of the

upper airways and cessation of airflow for at least

10 s during sleep. Obesity is believed to change upper-

airway anatomy through increased deposition of peri-

luminal fat. This leads to apnea, arterial hypoxemia,

recurrent arousals from sleep, excessive daytime som-

nolence, and snoring. OSA is more common among

the obese, with those having a BMI 30 or more being

tbl0001 Table 1 Classification of obesity according to the BMI

Classification BMI (kgm

2

)

Underweight <18.5

Normal 18.5–24.9

Overweight 25–29.9

Obesity

Class 1 30–34.9

Class 2 35–39.9

Class 3 >40

tbl0002Table 2 Relationship between waist circumference and the risk

of obesity-related complications

Risk

Waist circumference Low Moderate High

Men (in) <37 37–40 >40

(cm) <94 94–102 >102

Women (in) <32 32–35 >35

(cm) <80 80–88 >88

The high-risk cut off for men is a waist circumference of >102 cm (40 in),

and the high-risk cut off for women is a waist circumference of >88 cm

(35 in).

OBESITY/Etiology and Diagnosis 4225

at greatest risk. Patients with OSA can develop com-

plications like neuropsychiatric and behavioral dis-

turbances, systemic and pulmonary hypertension,

right heart failure, myocardial infarction and stroke.

There are data indicating that the symptoms of sleep

apnea improve with weight loss.

0057 Hypertension Obesity may influence the blood

pressure and predispose to hypertension. There is

strong and consistent evidence that weight loss

produced by lifestyle modifications reduces blood-

pressure levels.

0058 Dyslipidemia Obesity is associated with increased

total and low-density lipoprotein cholesterols,

increased serum triglycerides, and reduced levels of

protective high-density lipoprotein cholesterol. All

these lipid abnormalities are associated with an

increased risk of developing CAD.

0059 Other disease conditions associated with obesity

Other conditions include ischemic stroke, nonalco-

holic steatohepatitis, gallstones and cholecystectomy,

osteoarthritis, menstrual irregularities, and infertility.

Increased body weight is associated with an increased

risk for certain forms of cancer, including colon

cancer, endometrial cancer, and postmenopausal (but

not premenopausal) breast cancer. Maternal obesity

is a significant risk factor for the development of

gestational diabetes mellitus, and neural tube defects.

Physical examination and laboratory evaluation

0060 The physical exam should include, in addition to an-

thropometry, a pulse and blood pressure measure-

ment, examination of the thyroid, auscultation of

heart and lungs, palpation of the liver and examination

of weight-bearing joints. A laboratory evaluation will

help further in quantifying the risk of obesity-related

complications and in monitoring weight loss. It should

include serum chemistry, lipid profile and thyroid-

function tests. In certain high-risk individuals, an elec-

trocardiogram, stress test, chest X-ray, sleep study,

pulmonary-function tests, ultrasound of gallbladder,

liver, and ovaries, etc., may also be appropriate.

Conclusion

0061 The etiology of obesity has been discussed from sev-

eral perspectives. The concept of a genetic predispos-

ition to weight gain, the biological mechanisms

involved in the regulation of body weight, and its

individual variation have been discussed. This was

followed by a review of our current appreciation

of the regulation of energy balance, presented from

the point of view that small daily errors in positive

energy balance integrated over months and years

increasingly lead people to obesity. The complexity

of the interaction between genetics, behavior, and the

environment was also outlined.

0062Most available evidence indicates that higher

levels of body weight and body fat are associated

with an increased risk for the development of numer-

ous adverse health consequences. Medical history

should evaluate etiological factors that may have

played a role in the development of obesity. Physical

examination and laboratory tests should extend

this evaluation to risk factors associated with obesity.

See also: Cholesterol: Factors Determining Blood

Cholesterol Levels; Coronary Heart Disease: Etiology

and Risk Factor; Diabetes Mellitus: Etiology; Energy

Metabolism; Exercise: Metabolic Requirements;

Hormones: Steroid Hormones; Hypertension:

Physiology; Metabolic Rate; Obesity: Fat Distribution;

Treatment; Epidemiology

Further Reading

Anonymous (1998) Clinical Guidelines on the Identifica-

tion, Evaluation, and Treatment of Overweight and

Obesity in Adults – The Evidence Report. National

Institutes of Health (published erratum appears in

Obesity Research 1998 6: 464).

Astrup A (1998) The American paradox: the role of energy-

dense fat-reduced food in the increasing prevalence

of obesity. Current Opinion in Clinical Nutrition &

Metabolic Care 1: 573–577.

Bray GA (1999) Etiology and pathogenesis of obesity.

Clinical Cornerstone 2: 1–15.

Campfield LA and Smith FJ (1999) The pathogenesis of

obesity. Best Practice & Research Clinical Endocrin-

ology & Metabolism 13: 13–30.

Chagnon YC, Perusse L, Weisnagel SJ, Rankinen T and

Bouchard C (2000) The human obesity gene map: the

1999 update. Obesity Research 8: 89–117.

Flegal KM, Carroll MD, Kuczmarski RJ and Johnson CL

(1988) Overweight and obesity in the United States:

prevalence and trends, 1960–1994. International

Journal of Obesity & Related Metabolic Disorders 22:

39–47.

Hill JO and Peters JC (1998) Environmental contributions

to the obesity epidemic. Science 280: 1371–1374.

Hill JO, Wyatt HR and Melanson EL (2000) Genetic and

environmental contributions to obesity. Medical Clinics

of North America 84: 333–346.

Kopelman PG (2000) Obesity as a medical problem. Nature

404: 635–643.

Lonnqvist F, Nordfors L and Schalling M (1999) Leptin and

its potential role in human obesity. Journal of Internal

Medicine 245: 643–652.

Mokdad AH, Serdula MK, Dietz WH et al. (1999) The

spread of the obesity epidemic in the United States,

1991–1998. Journal of the American Medical Associ-

ation 282: 1519–1522.

4226 OBESITY/Etiology and Diagnosis

National Task Force on the Prevention and Treatment of

Obesity (2000) Overweight, obesity, and health risk.

Archives of Internal Medicine 160: 898–904.

Sheehan MT and Jensen MD (2000) Metabolic complica-

tions of obesity. Pathophysiologic considerations. Med-

ical Clinics of North America 84: 363–385.

Tremblay A (1999) Physical activity and obesity. Best Prac-

tice & Research Clinical Endocrinology & Metabolism

13: 121–129.

WHO (1998) Obesity: Preventing and Managing the

Global Epidemic. Geneva: World Health Organization.

Fat Distribution

F Deeb, Johns Hopkins Bayview Medical Center,

Baltimore, MD, USA

L J Cheskin, Johns Hopkins University, Baltimore,

MD, USA

Background

0001 While obesity is easily diagnosed in most cases, and is

well known to increase the risk of a variety of disease

conditions, less well appreciated is the basic physi-

ology of adipose tissue deposition and the effects of

different distributions of adipose tissue on heath risks.

Types of Human Obesity

0002 Obesity is defined as an excess of body weight as a

result of an excessive accumulation of fat and results

from interaction between the environment and genes.

A historically high-fat diet, in concert with decreasing

levels of physical activity, has recently resulted in an

epidemic of obesity and overweight in much of the

world, which now affects at least 64% of Americans.

Human adipose tissue can be classified by site into

four types: subcutaneous, yellow marrow, interstitial,

and visceral. Subcutaneous adipose tissue lies directly

under the dermis of the skin and superficial to the

fascia overlying the skeletal muscles. More than half

of total body fat is generally found in this site. Sub-

cutaneous adipose tissue can be further divided into a

deep layer and a superficial layer. One clinical study

found that during weight loss, the deep layer de-

creased to a greater extent than the superficial layer;

the significance of this finding is unknown.

0003 Interstitial adipose tissue is found between cells

and usually accounts for only a small proportion of

total body fat. Yellow marrow is the fat within the

bone marrow and is not normally subject to much

increase with weight gain.

0004Variation in the amount visceral adipose tissue

(VAT) has the greatest impact on health risks. VAT

can be subdivided into retroperitoneal and intraper-

itoneal adipose tissue. The intraperitoneal adipose

tissue can be further divided into mesenteric and

omental depots, whose veins drain into the portal

vascular system. The liver, too, may accumulate fat,

primarily within the hepatocytes. This may occur as a

benign result of weight gain (hepatic steatosis or

benign fatty liver) or as a manifestation of the often-

progressive disease known as nonalcoholic steato-

hepatitis (NASH), which is often accompanied by

obesity and /or type 2 diabetes.

0005A variety of terms have been used to define diff-

erences in adipose tissue accumulation patterns

including android/gynoid, apple/pear, central/periph-

eral, and upper body/lower body. Of note, typical

body-fat distribution differs between men and

women. Women tend to accumulate more lower-

body fat during weight gain, whereas men tend to

have upper-body abdominal accumulation of fat, as

well as variable lower-body fat accumulation. Purely

lower-body weight gain is not generally seen in non-

castrated males, though the typical male pattern of

predominantly upper-body weight gain is not infre-

quent in women.

0006The metabolic consequences of obesity are deter-

mined to some extent by the distribution of fat. A

number of animal and human studies have found that

central obesity poses a greater risk of, among other

conditions, cardiovascular disease, type-2 diabetes

mellitus, hypertension, gallstones, and gout com-

pared with the risk associated with peripheral obesity.

The amount of abdominal visceral fat appears to be

the most important corollary of health risk for the

individual with obesity. In fact, even in the absence of

overall obesity, an excess of VAT appears to be asso-

ciated with excess health risks.

Regulation of Adipose Tissue Distribution

in Humans

0007In view of the close epidemiologic and metabolic asso-

ciations between central obesity and disease, the regu-

lation of adipose tissue growth and distribution is

important to understand. Age and gender are two

important, nonmodifiable determinants of the size of

the VAT depot compared to subcutaneous fat. Increas-

ing age and male gender tend to increase VAT magni-

tude at a given level of total body fat. That is, weight

gain in general increases VAT, but to a lesser degree in

younger people and in women. However, genetic

factors account for a good deal of variability in the

amount of fat deposited in VAT or other sites. In add-

ition, some environmental (modifiable) factors appear

OBESITY/Fat Distribution 4227

important, and include smoking and lack of exercise. A

number of endocrine abnormalities have been variably

detected in association with central obesity, including

low testosterone secretion in men, elevated cortisol

and androgens in women, and low levels of growth

hormone in men and women. Hypersensitivity of the

hypothalamo–pituitary–adrenal (HPA) axis may be

the mechanism underlying these abnormalities. Insulin

resistance in peripheral tissues, leading to hyperinsuli-

nemia, also plays a key role. All of these hormonal

changes have important influences on adipose tissue

metabolism and distribution.

0008 At the adipocyte level, insulin and cortisol contrib-

ute to lipid accumulation by decreasing lipoprotein

lipase (LPL) activity. Growth hormone (GH) and

testosterone increase LPL activity, so that the de-

crease in these hormones often seen in central obesity

would also tend to decrease LPL activity and favor

further adipose tissue deposition. Because of the

higher blood flow, cellularity, and innervation in vis-

ceral compared with subcutaneous adipose tissues,

the consequences of the hormonal abnormalities de-

scribed above are believed to be expressed more in

visceral adipose tissue. Another factor accounting for

the disproportionate health effects of VAT is that the

number of androgen and cortisol receptors is higher

in VAT than other adipose tissue deposits. Thus,

endocrine abnormalities in VAT, e.g., elevated levels

of insulin and cortisol, which favor accumulation of

fat, and decreased levels of GH and sex hormones,

which mobilize fat, are magnified by the higher recep-

tor density, leading to further accumulation of fat in

VAT. In various physiological conditions associated

with increased visceral fat mass, the balance between

the lipid accumulation hormones (cortisol and insu-

lin) and the hormones that prevent lipid accumulation

and instead activate lipid mobilization (sex hormones

and GH) is shifted to favor the lipid-enhancing hor-

mones. Such conditions include polycystic ovary syn-

drome, Cushing’s syndrome, menopause, aging, GH

deficiency, HIV lipodystrophy, and excess alcohol

intake. Finally, local synthesis of steroid hormones in

adipose tissue may play a role in regulating deposition

of fat. Regional measurement of fat turnover reveals

higher rates of lipid mobilization in upper-body (vis-

ceral) adipose tissue than in lower-body adipose

tissue. The order in men is as follows: omental visceral

¼ retroperitoneal > subcutaneous abdominal > sub-

cutaneous femoral adipose tissue.

Effects of Fat Distribution on Health

0009 As noted, body fat distribution is now recognized as

an important predictor and modifier of many of the

adverse health consequences of obesity. Upper-body

obesity and abdominal visceral fat are associated

with a variety of metabolic complications, including

hypertension, insulin resistance, type-2 diabetes mel-

litus, dyslipidemia, gout, and premature coronary

death.

0010Evidence suggests that abnormally high adipose

tissue turnover in VAT, mediated by high levels of

LPL and/or increased sensitivity to catecholamines

or decreased sensitivity to insulin’s effect on in-

hibiting lipolysis, results in elevated free fatty acid

availability and may explain some aspects of the

metabolic consequences of upper-body obesity. Over-

all, though, the precise mechanism(s) by which excess

VAT lead to adverse health consequences is poorly

understood.

Heart Disease

0011Obesity is an independent risk factor for the develop-

ment of coronary artery disease (CAD). Obesity also

increases the risk of CAD indirectly through its ad-

verse effects on insulin resistance, lipid metabolism,

and blood pressure. Central obesity is the pattern

most highly correlated with an adverse coronary

risk profile. Treatment of obesity results in an im-

proved coronary risk profile. Despite the high preva-

lence of obesity in coronary populations, the effect of

weight loss on hard cardiovascular outcomes such as

myocardial infarction and death has received rela-

tively little attention.

Endocrine Abnormalities

0012The endocrine and metabolic complications most fre-

quently seen in obesity are insulin resistance, type 2

diabetes mellitus, dyslipidemia, menstrual abnormal-

ities, and infertility.

0013Insulin resistance is quite common in severe

obesity, and occurs especially with central obesity.

Insulin resistance is a central pathophysiologic fea-

ture of multiple conditions, the conglomeration of

which is referred to as ‘Syndrome X.’ Syndrome X

includes hyperglycemia, hyperinsulinemia, dyslipide-

mia, and hypertension, which are associated with an

increased risk of CAD and stroke. HPA axis hyper-

sensitivity, as evidenced by an increased response to

challenges at all levels of the HPA axis, from the

adrenals to the central regulatory centers, appears to

be associated with obesity, in particular, central

obesity. Sex steroid and GH secretions are blunted,

despite heightened HPA reactivity. The hyperandro-

genicity frequently seen in obese women may be

related to increased testosterone production in the

ovaries and adrenals.

0014Obesity in girls is associated with early menarche

and puberty. The effect of childhood obesity on boys

is more variable; obesity can lead to either early or

4228 OBESITY/Fat Distribution

delayed puberty. Pubertal gynecomastia is a common

problem in obese boys.

Gastrointestinal Conditions

0015 A gastrointestinal disorder for which obesity is a

classical risk factor is cholelithiasis. The magnitude

of risk is directly related to the severity of obesity but

probably not to fat distribution. Since, for each

kilogram of fat gained, an additional 20 mg of chol-

esterol is synthesized and excreted in the bile, this

increased cholesterol turnover is the probable mech-

anism by which obesity increases the likelihood of

precipitation of cholesterol gallstones. The risk for

gallbladder stones increases during weight loss be-

cause of unfavorable changes in bile composition

(lithogenicity), increases in the flux of cholesterol

through the bile ducts as fat is mobilized, and

decreased gallbladder contractility. New gallstone

formation especially occurs in subjects who experi-

ence rapid weight loss after gastric surgery for obesity

or after dieting with a very-low-calorie (< 800 kcal -

per day) and low-fat diet (as many as 25–35% of

patients in some studies develop usually asymptom-

atic gallstones). The risk for gallstones appears to be

lower in patients consuming a low calorie diet

(800 kcal per day) containing 15–25 g of fat per day

(4% after 10 weeks of dieting).

0016 NASH, a liver disease with frequent sequelae of

fibrosis and cirrhosis, occurs most commonly among

obese patients and those with type 2 diabetes, and

thus is likely to be more common in central obesity.

Alanine and aspartate aminotransferase and alkaline

phosphatase are the most commonly elevated liver

enzyme levels in NASH but are usually no more

than twice the upper limit of normal and do not

correlate well with histological abnormities. The

pathogenesis of liver injury in obese individuals with

NASH is in part secondary to the proinflammatory

cytokine, tumor necrosis factor a (TNF-a), which has

emerged as a key factor in various forms of liver

disease. Data from animal and clinical studies suggest

that TNF-a mediates not only the early stage of fatty

liver but also the transition to more advanced stages

of liver damage. A modest weight loss (> 10% of body

weight) can normalize liver tests, decrease liver fat

content, and decrease liver size.

0017 Another common gastrointestinal condition asso-

ciated with obesity is gastroesophageal reflux disease

(GERD). Abdominal obesity (and pregnancy) are

especially associated with GERD, as these condi-

tions result in increased intra-abdominal pressure,

which is a central mechanism for reflux of gastric

contents into the acid-sensitive esophagus. Abdom-

inal hernias are also associated in particular with

central obesity.

Pulmonary Conditions

0018Pulmonary conditions associated with obesity in-

clude obstructive sleep apnea (OSA) and obesity-

hypoventilation syndrome (OHS). In OSA, patients

suffer from repeated attacks of upper-airway obstruc-

tion during sleep. OSA is fat distribution-sensitive

because it is believed to be associated with increased

fat deposition in the tongue, uvula, pharynx, and

hypopharynx. OHS is a condition associated with

serious obesity in which an awake patient suffers

from hypercarbia and hypoxemia. Abdominal obesity

is a mechanical factor in the etiology of OHS, since

increased abdominal fat tends to raise the diaphragm,

as well as increase fat deposition within the dia-

phragm and intercostal muscles, and also increase

chest-wall weight. Leptin, a protein produced by adi-

pose cells, serves as a pulmonary growth factor and as

a modulator of the central respiratory control center.

Leptin deficiency or, more likely, leptin resistance is

believed to play a role in OHS and OSA.

Assessment of Human Obesity

0019In order to assess an individual’s body fat content and

fat topography, a comparison of measures obtained in

the individual with age- and gender-specific norms is

necessary. This procedure has proved to be challen-

ging in both clinical and research settings. At least

three body-fat measures (total body fat content,

upper-body fat, abdominal visceral fat) are very im-

portant, and must be evaluated not just in a labora-

tory environment but also in the physician’s office

and in large-scale population studies. Table 1 lists

the current methods available to obtain a direct or

predicted measure of total body fat content.

0020Anthropometry is the cheapest, most widely used

method of assessing human-body composition. An-

thropometry measurements can be used both clinic-

ally and in epidemiological studies to grade the degree

of adiposity in either individuals or groups. The meas-

urements are also used to describe the anatomic

distribution of adipose tissue and thus classify indi-

viduals and groups with regard to the type of obesity

(central or peripheral). The anthropometric measures

considered most useful in assessing obesity include

weight, stature, skinfold thickness, and circumference

of the trunk and limbs.

Weight

0021Body weight is best measured to the nearest + 0.1 kg

using a beam-balanced scale. Despite the requirement

of frequent and careful calibration, spring scales or

electronic scales may be used instead. Patients should

OBESITY/Fat Distribution 4229

be measured either nude or wearing light clothing of

known weight.

Stature

0022 The preferred method of measuring stature is by

using a wall-mounted stadiometer, measuring to the

nearest + 1 cm. Plastic stadiometers are available for

clinical use that have acceptable accuracy. The pos-

ition of the patient is very important and should be

standardized, the patient standing erect with the

head, shoulders, and buttocks against the stadiometer

wall. Body weight and stature can be used to calculate

the body-mass index (BMI) (or Quetelet’s index)

or weight corrected for height and to compare

this value to percentiles for the distribution of this

index by sex, age, and race tabulated from large

surveys conducted by the National Center for Health

Statistics. The BMI is calculated as the weight (in

kilograms) divided by the square of height (in meters)

or as the weight (in pounds) multiplied by 704 and

divided by the square of the height (in inches). It is

important to remember that age and body proportion

(leg/trunk length ratio) influence the correlation of

BMI with height and that BMI is correlated with

lean as well as fat mass. This means that a very

muscular individual will have a measured BMI that

puts them in the obese category, although they do not

necessarily have an abnormal percentage of body

weight composed of fat.

Skinfold Thickness

0023 This is a measurement of a double thickness or ‘fold’

of skin, including the underlying fascia and subcuta-

neous adipose tissue, which is taken using calipers

at standard locations on the body. It is performed

by pinching and elevating a skinfold at a specific

anatomical site using the thumb and forefingers, and

measuring the thickness of the fold with a specially

designed caliper. The anatomic sites commonly meas-

ured are the triceps (midway between the shoulder

and the elbow), the subscapular, suprailiac and para-

umbilical area, and the medial thigh and calf. These

measurements correlate with, but do not accurately

measure, the actual mean thickness of the subcutane-

ous adipose tissue. This has been illustrated by com-

parisons of caliper skinfold thickness measurements

with radiographic and ultrasound measurements of

the true subcutaneous adipose tissue thickness at

different anatomic sites. Reproducible skinfold

measurement requires training. A major criticism of

skinfold thickness methods is that they ignore vari-

ations in the amounts of internal adipose tissues,

especially the visceral adipose tissue that is associated

with so many of the increased health risks of obesity.

Circumferences

0024Body circumferences can be measured more easily in

severely obese patients than skinfold thickness. Cir-

cumferences have an additional advantage over skin-

fold thicknesses in that they can measure internal as

well as subcutaneous adipose tissue. However, unlike

skinfold measures, circumferences are influenced by

variation in the size of underlying muscles and bone.

The most useful circumferences for grading or pre-

dicting body fat and for describing adipose tissue

distribution are the upper arm, chest, waist or abdo-

men, hip or buttocks, and the thigh (proximal or

midthigh). In men, the waist circumference is highly

correlated with total body fat. In women, the hip or

thigh circumference is more predictive of total body

fat. Many circumference indices have been devised

in an effort to capture the association between

tbl0001 Table 1 Methods of estimating body fat and its distribution

Method Cost Ease of use Accuracy Measure of regional fat

Height and weight $ Easy High No

Skinfolds $ Easy Low Yes

Circumferences $ Easy Moderate Yes

Ultrasound $$ Moderate Moderate Yes

Density/immersion $ Moderate High No

Heavy water

Tritiated $$ Moderate High No

Deuterium oxide or heavy oxygen $$$ Moderate High No

Potassium isotope (40K) $$$$ Difficult High No

Total body electrical conductivity $$$ Moderate High No

Bioelectric impedance $$ Easy High No

Absorptiometry (dual-energy X-ray absorptiometry) $$$ Easy High Yes

Computed tomography $$$$ Difficult High Yes

Magnetic resonance imaging $$$$ Difficult High Yes

Neutron activation $$$$ Difficult High No

Adapted from Bray GA and Gray DS (1988) Obesity. Part I – Pathogenesis. Western Journal of Medicine 149(4): 429–441.

4230 OBESITY/Fat Distribution

fatty-tissue distribution and morbidity and mortality.

The most popular circumference index is the ‘waist/

hip ratio’ (WHR), followed by the ‘waist/thigh ratio’

(WTR). The WHR is an independent predictor of

metabolic disturbance including insulin resistance,

hyperlipidemia, hypertension, and arteriosclerosis.

Similar associations have been reported for WTR, as

well as for skinfold thickness indices. Recent evidence

suggests, however, that the waist circumference alone

is as reliable as the WHR in predicting VAT and its

associated health risks.

Ultrasound

0025 Ultrasound has the advantages of measuring subcuta-

neous adipose tissue thickness more accurately than

skinfold measures and of being able to measure other-

wise inaccessible sites. The two major disadvantages

of ultrasound are that an experienced technician is

usually required and that the costs are high.

Hydrodensitometry

0026 An obese person floats higher in water than a non-

obese person. This is because the density of fat

mass is lower than that of fat-free mass (FFM).

Underwater weighing is one of the oldest in vivo

methods of analyzing human-body composition as a

two-compartment (fat and fat-free body mass) model.

It held the status of being the ‘gold standard’ for

body-fat composition analysis for many years but is

both inconvenient and not as precise a measure of

body composition as other methods.

Bioimpedance and Conductivity

0027 Total body electrical conductivity and bioelectrical

impedance are techniques for predicting body

composition based on the measurement of the elec-

trical resistance in the body to a tiny current. This

electrical resistance is proportional to body shape and

the volume of conductive tissue (body components

with high water concentrations such as the FFM and

skeletal-muscle mass). As a result, these methods do

not estimate body fatness but instead predict FFM; fat

must be derived secondarily as the difference between

the predicted FFM and the body weight. These tests

have the advantage of being simple, quick, and

inexpensive, and can be readily used in population

studies. Their disadvantages are the variability in the

measurement and its dependence on the hydration

level of the patient.

Absorptiometry

0028 Dual-energy X-ray absorptiometry (DEXA) was pri-

marily designed to measure the amount of mineral

within bone, but can also be used to estimate the

amount of fat in soft tissues. DEXA is an outgrowth

of dual-photon absorptiometric systems, having been

introduced in the early 1990s as faster and more

accurate. DEXA is quick and simple to carry out,

yields information about regional adipose tissue

distribution, because it is a whole body scan, but

is costly.

Imaging

0029Imaging studies, such as computed tomography and

magnetic resonance imaging (MRI), are widely con-

sidered the most accurate means currently available

for assessing body-fat distribution, but the limitations

are the high cost, expertise needed, radiation expos-

ure, and limited utility in a research setting. These are

the only methods available for precise, accurate quan-

tification of visceral and other internal depots of

adipose tissue. MRI is now the method of choice

for calibration of field methods of measuring body

fat and skeletal muscles in vivo.

Isotope Dilution

0030Dilutional methods include a group of specialized

research techniques for measuring body composition

of fluid compartments (e.g., total body water (TBW),

extracellular fluid, and plasma volume) and the

electrolytes within those compartments, such as

exchangeable potassium, sodium, and chlorine. They

are costly, require specialized training, and are not

widely available. Examples are heavy water and

neutron activation measures.

Heavy Water

0031Water labeled with either two isotopes of hydrogen

(deuterium, 2H

O; tritium, 3H

O) or oxygen (H

has been used to quantitate TBW by a dilution

method in healthy and diseased individuals.

Neutron Activation

0032Whole-body counting /in vivo neutron activation an-

alysis can be used to estimate adiposity components.

This method enables all main anatomic elements to

be quantified at the anatomic level in vivo. Once the

elements have been measured, the proportion of fat,

protein, water, and mineral can be calculated by

applying simultaneous equations. These techniques

are not widely available but are precise.

0033In summary, an increasingly well-recognized and

understood modifier of health risk in obesity is

regional fat distribution. While the ideal method of

measuring fat distribution has not been defined,

efforts should be made to identify those individuals

who are at high risk because of an unfavorably

high VAT mass. As a marker of health risk, regional

OBESITY/Fat Distribution 4231

distribution of fat is arguably more important

than obesity per se, and should be afforded the prom-

inence it warrants in the evaluation and treatment of

obesity.

See also: Body Composition; Coronary Heart Disease:

Etiology and Risk Factor; Diabetes Mellitus: Etiology;

Hormones: Pituitary Hormones; Nutritional

Assessment: Importance of Measuring Nutritional

Status; Anthropometry and Clinical Examination;

Obesity: Etiology and Diagnosis