An Understanding of Body Weight

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Total body weight is usually thought of as a series of compartments. Gain or loss of weight should be thought of in terms of how much is added to or lost from each compartment.

One scheme is to think of the body as water and everything else: water makes up approximately 60% of the total body mass in men, slightly less in women, and it decreases with age in both sexes. The higher the proportion of body fat, the lower the proportion of water. Body water is divided into two large compartments, the intracellular water (66%) and the extracellular water (34%); it is important to note that the extracellular water is essentially saline with a sodium concentration of approximately 140 mEq/L, while the intracellular water is rich in potassium and relatively low in sodium. The extracellular compartment is further divided into the extravascular fluid (75%) and the intravascular fluid (25%) most of which is in the capacitance veins.

Another scheme is to visualize the body as a series of tissue compartments. There is a relatively stable component forming the visceral organs and skeleton, which vary little in mass, and a variable component made up largely of extracellular fluid, skeletal muscle, and fat. Therefore, when faced with inappropriate or unexpected changes in weight, the clinician should try to determine which combinations of changes in body water, muscle and fat have occurred. This will help in determining the specific etiology of the change observed.

Weight should be measured at each visit to establish a baseline range and to detect any significant changes. Weight is measured on a scale, the most accurate being a calibrated balance scale. Properly calibrated electronic scales are quite accurate. Weight is recorded in pounds or kilograms, preferably without heavy clothing or shoes.

Body Mass Index

The body mass index (BMI) is a standardized measure of the relationship of body mass to height. It has allowed for the calculation of the risk for adverse events in populations with different BMIs. The BMI is calculated by dividing the weight in kilograms by the (height in meters)2; the units are thus kg/m2. The upper limit of normal was identified as the point at which the risk for adverse health outcomes began to rise; the lower limit was similarly determined. The BMI does not distinguish increases in lean body mass from increases in fat mass.


Growth charts using the BMI have been developed and are being used increasingly in well-child care. Calculation of BMI and setting weight loss goals based on the BMI are clinically useful; it allows patients to compare themselves with other individuals and the population risks associated with their current and target BMI.

Waist-Hip Ratio

Women have more subcutaneous fat than men, and they tend to distribute increased adipose tissue more diffusely, predominately in the subcutaneous fat. Men, especially those who gain weight in mid-life, tend to develop visceral adiposity in the internal organs and omentum; this adipose tissue is metabolically different from the subcutaneous fat and appears to play a pathophysiologic role in the increased incidence of hyperlipidemia and insulin resistance in these individuals. The waist: hip ratio (the ratio of the body circumference at the hip and waist) has been used to quantify this type of fat distribution. Abnormal waist-hip ratio is >0.9 for women and >1.0 for men; abnormal waist circumference is >40 inches (90 cm) for men or >35 inches (80 cm) for women. An increased waist-hip ratio or waist circumference correlates with risks of adverse health even and appears to be a better predictor than BMI [Yusuf S, Hawken S, Ounpuu S, et al. Obesity and the risk of myocardial infarction in 27 000 participants from 52 countries: A case-control study. Lancet. 2005;366:1640–1649 [PMID: 16271645]; Romero-Corral A, Montori VM, Somers VK, et al. Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: A systematic review of cohort studies. Lancet. 2006;368:666–678 [PMID: 16920472].

Key Syndrome Growth Retardation—Cystic Fibrosis

Any of several autosomal recessive mutations of the epithelial chloride channel gene leads to a production of viscous mucus by the exocrine glands. This results in chronic progressive dysfunction of the pancreas and lungs. Patients are usually diagnosed in childhood, although some, with more mild mutations, escape detection until adulthood. Symptoms include bulky, foul-smelling stools, cough, and dyspnea. Pancreatic obstruction leads to maldigestion and growth retardation. Lung involvement produces a cough and recurrent pulmonary infections, often leading to chronic infection with Pseudomonas aeruginosin and bronchiectasis. Involvement of the sweat glands makes affected individuals very susceptible to salt and water losses in warm environments. Complications include fecal impactions, intussusception, volvulus, and chronic bronchitis. With advanced pulmonary disease, cardiomegaly and clubbing of the fingers are present.

Key Sign Weight Loss

Weight loss occurs when energy (calorie) utilization or loss exceeds intake. It can arise from decreased effective intake (net of ingestion, emesis and stool losses), maldigestion, malabsorption, increased metabolic utilization, or increased losses of calories. Failure to gain weight and grow appropriately in childhood and adolescence has the same significance as weight loss in the adult. The history is most useful in formulating a probable pathophysiology. Ask the patient’s estimate of the weight lost over a specific time and obtain records of weight to validate the history. Ask whether the patients clothes fit differently or if family or friends have noted a change in appearance. Review the patient’s daily intake of food and drink, and determine if there has been a change in activities. Look at the patient’s belt to see if there is a change in the pattern of wear. Look for a strike and loose skin over the abdomen and arms. Often more than one mechanism is at work, for example decreased intake and increased utilization [Bouras EP, Lange SM, Scorpio JS. A rational approach to patients with unintentional weight loss. Mayo Clin Proc. 2001;76:923–929 [PMID: 11560304]; Detsky AS, Smalley PS, Chang J. The rational clinical examination. Is this patient malnourished? JAMA. 1994;271: 54–58 [PMID: 8258889]. DDX: Weight loss without a decrease in intake suggests impaired nutrient assimilation (maldigestion, malabsorption), glucosuria (diabetes mellitus), or increased metabolic rate (hyperthyroidism, pheochromocytoma). Cancer and psychosocial problems, especially depression, are the two most prevalent explanations.


Endocrine hyperthyroidism, adrenal insufficiency, diabetes (especially type 1); Idiopathic advanced age (normal adults lose weight gradually after age 60 years), any debilitating disease; Inflammatory any systemic inflammatory disease, for example, SLE, RA, vasculitis; Infectious chronic disseminated infection or advanced local infection, for example, tuberculosis, chronic active hepatitis, AIDS, intestinal parasites; Metabolic/Toxic organ failure (uremia, advanced liver disease, emphysema, congestive heart failure), increased physical activity, maldigestion and malabsorption, dieting, decreased intake and starvation; Mechanical/Traumatic bowel obstruction, dysphagia, odynophagia, dental and chewing problems, decreased mobility, paralysis, apraxia; Neoplastic cancers decrease appetite and increase utilization, especially when disseminated or involving the liver; Neurologic hypothalamic disorders; Psychosocial dieting, dementia, depression, anorexia nervosa, bulimia, abuse, isolation, poverty; Vascular vasculitis, multi-infarct dementia.


Cytokines released in chronic infections and in the presence of malignancies lead to wasting of muscle protein and increased metabolic demands resulting in profound weight loss and redistribution. Cachexia is physiologically distinct from starvation and cannot be reversed by refeeding. Cachexia is classically seen in chronic tuberculosis (consumption) and slow growing visceral malignancies (e.g., advanced pancreatic and colon cancers), but any chronic disease with persistent activation of the immune system may produce the syndrome [Kotler, DP. Cachexia. Ann Intern Med. 2000;133;622–634]. CLINICAL OCCURRENCE: common associations are HIV-AIDS, CHF, advanced liver and renal disease, RA, Addison disease, chronic obstructive pulmonary disease and advanced age.

Key Sign Weight Gain

Weight increases whenever the intake of calories exceeds the metabolic demands, or when calorie-free salt and water are retained. Therefore, weight gain can occur from increased intake, decreased metabolic demands, and/or renal retention of salt and water. Weight gain is a part of normal growth and failure to gain weight appropriately during childhood and adolescence is abnormal. Once skeletal maturity is reached, weight gain continues for a variable length of time as skeletal muscle mass increases to adult size, this is especially true in men. After reaching adult mass in the early twenties, any further increase in weight indicates a pathologic condition, a decrease in physical exercise, or an increase in caloric intake. Fats and alcohol have the highest energy content, 9 and 7.5 kcal/g respectively, whereas the energy content of carbohydrates and protein is 4.5 kcal/g. A careful dietary and exercise history should be obtained. Also, inquire about changes in appetite, libido, skin, hair, and bowel habits. Note the pattern of weight gain during the physical examination and any evidence of retention of extracellular fluid as edema. CLINICAL OCCURRENCE: Increased Intake overeating, mild hyperthyroidism, insulinoma, hypothalamic injury, treatment of diabetes, anabolic steroids; Decreased Metabolic Demands hypothyroidism, hypogonadism, inactivity, confinement; Salt and Water Retention congestive heart failure, kidney failure, nephrotic syndrome, hepatic insufficiency, portal hypertension with ascites, idiopathic edema, diuretic rebound, venous insufficiency with dependent edema.

Key Syndrome Obesity

Genetics and lifestyle each play important roles in the development of obesity. Caloric intake in excess of expenditures will lead to weight gain, but obesity requires the failure of a feedback loop to control intake; the cause(s) of this failure are unknown. Obesity is epidemic in the United States; fully a third or more of the adult population is obese. There is a strong correlation of obesity with insulin resistance and the development of hypertension, diabetes, heart disease, cancer, and overall mortality. Obesity is readily recognized and diagnosed, but is very difficult to treat, especially if onset is in childhood or adolescence. Obesity can result from the causes of weight gain, but more commonly the exact factors leading to the marked gain in body weight, beyond dietary and exercise habits, are obscure [Haslam DW, James WPT. Obesity Lancet. 2005;366:1197–1209 [PMID: 16198769]; Yanovski SZ, Yanovski JA. Obesity. N Engl J Med. 2002:346:591–602]. DDX The distribution of adipose tissue assists diagnosis. Truncal obesity with thin limbs, round facies and a prominent hump of fat on the upper back are characteristic of Cushing disease, iatrogenic steroid use and, more recently, the use of protease inhibitors in the treatment of HIV-AIDS. Localized accumulations of fat are seen at sites of repetitive insulin injection (lipodystrophy). Abdominal obesity tends to be seen in men with mid-life weight gain (beer belly).

Key Syndrome Metabolic Syndrome

The clustering of specific conditions with an increased risk for diabetes and cardiovascular disease has been labeled the metabolic syndrome. The cause is unknown, but obesity and insulin resistance play large roles. The definitions have been evolving and a new consensus definition was published in 2005. The diagnosis is based upon increased waist circumference, plus any two of the following: elevated triglycerides (>150 mg/dL) or treatment of hypertriglyceridemia; reduced HDL-cholesterol (men <40 mg/dL, women <50 mg/dL) or treatment for low HDL; elevated BP (systolic 130 mm Hg, diastolic 85 mm Hg) or treatment of hypertension; elevated fasting plasma  (100 mg/dL) or previously diagnosed type 2 diabetes [Alberti KG, Zimmet P, Shaw J. The metabolic syndrome—a new worldwide definition. Lancet. 2005;366:1059–1062 [PMID: 16182882]; Eckel RH, Grundy SM, Zimmet PZ. The metabolic syndrome. Lancet. 2005;365:1415–1428 [PMID: 15836891].

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