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An individual’s weight and body composition (proportion of fat and fat distribution) offer information about health status and may provide a clue to the presence of disease when out of balance. Nutrition is considered the science of food as it relates to promoting optimal health and preventing chronic disease. Nutritional intake and status offer insight into an individual’s health status. A nutritional assessment is an analysis of an individual’s approximate nutrient intake and relates it to the history, physical examination findings, body size measurements, and biochemical measures. This chapter focuses on the assessment of an individual’s body size and nutritional status and the examination for growth, gestational age, and pubertal development.
From the history and physical examination, assess the patient’s nutritional status, including:
Recent growth, weight loss, or weight gain
Chronic illnesses affecting nutritional status or intake
Medication and supplement use
Assessment of nutrient intake
Obtain the following body size measurements and compare them to standardized tables:
Standing height
Weight
BMI
Waist circumference
Calculate waist-height ratio
In this chapter, the terms “female” and “male” are used in order to differentiate between the body composition, physical and sexual development, and growth measurements in patients assigned as female or male at birth, respectively. This becomes important to the examination and health assessment of patients who are transgender male, transgender female, and non-binary.
Food nourishes the body by supplying necessary nutrients and calories to function in one or all of three ways:
To provide energy for necessary activities
To build and maintain body tissues
To regulate body processes
The nutrients necessary to the body are classified as macronutrients (carbohydrates, protein, and fat), micronutrients (vitamins, minerals, and electrolytes), and water. Energy requirements are based on the balance of energy expenditure associated with body size, composition, and the level of physical activity. An appropriate balance contributes to long-term health and allows for the maintenance of optimal physical activity. Adequate nutrition, from a well-balanced diet, supports growth, the increase in size of an individual, or of a single organ. Growth is also dependent on a sequence of endocrine, genetic, environmental, and nutritional influences.
Many hormones must interact and be in balance for normal growth and development to proceed ( Fig. 8.1 ). Two hypothalamic hormones control growth hormone synthesis and secretion in the anterior pituitary gland. Growth hormone–releasing hormone (GHRH) stimulates the pituitary to release growth hormone. Somatostatin, or growth hormone–inhibiting hormone (GHIBH), inhibits the secretion of both GHRH and thyroid-stimulating hormone (TSH). Growth hormone is secreted in pulses, with 70% of secretion occurring during deep sleep ( Sam and Frohman, 2008 ). Growth hormone promotes growth and increases in organ size, and it regulates carbohydrate, protein, and lipid metabolism.
Thyroid hormone stimulates growth hormone secretion and the production of insulin-like growth factor 1 (IGF-1) and interleukins 6 and 8 (IL-6 and IL-8), which have important roles in bone formation and resorption. The thyroid hormone also affects the growth and maturation of other body tissues.
IGF-1 is a growth hormone produced by the liver and in peripheral tissues, like bone. Through activation of IGF-1 receptors throughout the body, IGF-1 exerts a negative feedback effect on growth hormone secretion and mediates the effect of growth hormone on bone, muscle, nervous system, and immune system cells (Werner et al., 2008). Ghrelin, a peptide, known as the “hunger hor mone,” helps control growth hormone release and influences food intake and obesity development ( Sakata and Sakai, 2010 ).
Leptin has a key role in regulating body fat mass, and its concentration is thought to be a trigger for puberty by informing the central nervous system that adequate nutritional status and body fat mass are present to support pubertal changes and growth ( Low, 2011 ). Before puberty, body composition does not differ much between males and females. During puberty, with an increase in leptin, a relative decrease in fat percentage develops in males and an increase occurs in females ( Rogol, 2010 ). During puberty, the gonads begin to secrete testosterone and estrogen. Rising levels of these hormones trigger the release of gonadotropins (luteinizing hormone [LH] and follicle-stimulating hormone [FSH]) from the hypothalamus that stimulates the gonads to release more sex hormones. The genitalia begin growing to adult proportions. Testosterone enhances muscular development and sexual maturation and promotes bone maturation and epiphyseal closure. Estrogen stimulates the development of female secondary sexual characteristics, regulating the timing of the growth spurt and the acceleration of skeletal maturation and epiphyseal fusion. Androgens, secreted by the adrenal glands, promote masculinization manifested by secondary sex characteristics and skeletal maturation.
Growth at puberty is dependent on the interaction of growth hormone, IGF-1, leptin, and sex steroids (androgens). The sex steroids stimulate an increased secretion of growth hormone, which in turn mediates the dramatic increase in IGF-1. This leads to the adolescent growth spurt.
Each organ or organ system has its particular period of rapid growth marked by rapid cell differentiation. Each individual has a unique growth timetable and final growth outcome, but the sequential growth patterns are consistent. An external environmental or abnormal pathophysiologic process may intervene and influence the expected growth pattern ( Fig. 8.2 ).
The growth of the musculoskeletal system and most organs such as the liver and kidneys follows the growth curves described for stature. Skeletal growth is considered complete when the epiphyses of long bones have completely fused during late puberty. More than 90% of the skeletal mass is present by 18 years of age ( Reiter and Rosenfield, 2008 ).
Weight is closely related to growth in stature and organ development. Growth and development are influenced by nutritional adequacy, which contributes to the number and size of adipose cells. The number of adipose cells increases throughout childhood. Gender-related differences in fat deposition appear in infancy and continue through adolescence.
Lymphatic tissues (i.e., lymph nodes, spleen, tonsils, adenoids, and blood lymphocytes) are small in relation to total body size but are well developed at birth. These tissues grow rapidly to reach adult size by 6 years of age. By age 10 to 12 years, the lymphatic tissues are at their peak, about double adult size. During adolescence, they decrease to adult size.
The internal and external reproductive organs grow slowly before puberty. The reproductive organs double in size during adolescence, achieving maturation and function.
The brain, along with the skull, eyes, and ears, completes physical development more quickly than any other body part. The most rapid and critical period of brain growth occurs between conception and 3 years of age. By 34 weeks’ gestation, 65% of the weight of a newborn’s brain is present. Gray matter and myelinated white matter increase dramatically between the 34th and 40th weeks of gestation. At the time of full-term birth, the brain’s structure is complete and an estimated 1 billion neurons are present. Glial cells, dendrites, and myelin continue to develop after birth, and by 3 years of age, most brain growth is completed ( Fiegelman, 2011 ). The head circumference increases in infants and toddlers as brain growth occurs. During adolescence, the size of the head further increases because of the development of air sinuses and the thickening of the scalp and skull.
As infants and children grow, the change in body proportion is related to the pattern of skeletal growth ( Fig. 8.3 ).
Growth of the head predominates during the fetal period. Fetal weight gain follows growth in length, but weight reaches its peak during the third trimester with the increase in organ size. An infant’s birth weight is influenced by genetic predisposition, gestational age, the mother’s prepregnancy weight, weight gain during pregnancy, environmental exposures like secondhand smoke, overall maternal health, and intercurrent disease or complications in pregnancy such as gestational diabetes.
During infancy, the growth of the trunk predominates. Weight gain is initially rapid, but the speed with which weight is gained decreases over the first year of life. The fat content of the body increases slowly during early fetal development and then increases during infancy.
The legs are the fastest-growing body part during childhood, and weight is gained at a steady rate. Fat tissue increases slowly until 7 years of age, at which time a prepubertal fat spurt occurs before the true growth spurt.
The trunk and the legs lengthen during adolescence and lean body mass averages 80% in males and females ( Cromer, 2011 ). During adolescence, about 50% of the individual’s ideal weight is gained, and the skeletal mass and organ systems double in size.
During adolescence, males develop broader shoulders and greater musculature; females develop a wider pelvic outlet. Males have a slight increase in body fat during early adolescence and then have an average gain in lean body mass to 90%. Females accumulate subcutaneous fat and have a slight decrease in lean body mass to an average of 75% ( Cromer, 2011 ).
Progressive weight gain is expected during pregnancy, but the amount varies among patients. The growing fetus accounts for 6 to 8 pounds of the total weight gained. The remainder results from an increase in maternal tissues:
Fluid volume—2 to 3 pounds
Blood volume—3 to 4 pounds
Breast enlargement—1 to 2 pounds
Uterine enlargement—2 pounds
Amniotic fluid—2 pounds
Maternal fat and protein stores—4 to 6 pounds
The rate of desirable weight gain follows a curve through the trimesters of pregnancy, slowly during the first trimester and more rapidly during the second and third trimesters. Maternal tissue growth accounts for most of the weight gained in the first and second trimesters. Fetal growth accounts for most weight gained during the third trimester.
Maternal nutrition before and during pregnancy and during lactation may have subtle effects on the developing brain of the infant and on the outcome of the pregnancy. Patients who have inadequate weight gain are at greater risk for delivering a low-birth-weight infant. Epigenetic research is revealing the potential consequences of inadequate maternal nutrition on the adult health of the fetus ( Box 8.1 ).
Epigenetic research is revealing an association between an individual’s genome and environmental exposures during fetal life and adult health. Undernutrition during the second and third trimesters of pregnancy is believed to influence the fetus during the critical growth stages. Undernutrition (poor maternal nutrition or poor intrauterine environment) stresses the fetus, leading to adaptive and permanent changes in the infant’s endocrine and metabolic processes. Restricted fetal growth and a low birth weight for gestational age are associated with increased adult cardiovascular risk factors such as hypertension, insulin resistance, and abnormal lipid metabolism. These risk factors are further influenced by nutrition and growth after birth. Increased nutrition can lead to compensatory growth in these higher-risk infants during the first 2 years of life, resulting in a child who has an increased body mass index and body fat by 5 years of age.
Postpartum weight loss often occurs over the first 6 months after birth, with most weight loss occurring by 3 months after delivery. Patients who gained more than the recommended weight during pregnancy are less likely to return to their prepregnancy weight. They may be susceptible to future obesity and its health consequences.
Physical stature declines in older adults beginning at approximately 50 years of age. The intervertebral disks thin and kyphosis develops with the potential of osteoporotic vertebral compression.
Individuals older than 60 years often have a decrease in weight for height and BMI and a loss of 5% body weight over several years. An increase in body fat also occurs as skeletal muscle declines and anabolic steroid secretion is reduced. Older adults also frequently have decreased physical activity, which contributes to skeletal muscle loss with an associated increased risk for poor function and disability (Kalyani et al., 2014). Physical activity recommendations vary by age. See Table 8.1 for guidelines for physical activity by age group from the U.S. Department of Health and Human Services (HHS).
Age | Recommendations |
---|---|
3–5 years | Preschool-aged children should be physically active throughout the day (ideally 3 hours per day of active play and structured activities). |
6–17 years | Children and adolescents should do 60 minutes or more of physical activity daily.
|
18–64 years |
|
65 years and older |
|
a Moderate-intensity physical activity: Aerobic activity that increases a person’s heart rate and breathing to some extent. On a scale relative to a person’s capacity, moderate-intensity activity is usually a 5 or 6 on a 0 to 10 scale. Brisk walking, dancing, swimming, or bicycling on a level terrain are examples.
b Vigorous-intensity physical activity: Aerobic activity that greatly increases a person’s heart rate and breathing. On a scale relative to a person’s capacity, vigorous-intensity activity is usually a 7 or 8 on a 0 to 10 scale. Jogging, singles tennis, swimming continuous laps, or bicycling uphill are examples.
c Muscle-strengthening activity: Physical activity, including exercise that increases skeletal muscle strength, power, endurance, and mass. It includes strength training, resistance training, and muscular strength and endurance exercises.
d Bone-strengthening activity: Physical activity that produces an impact or tension force on bones, which promotes bone growth and strength. Running, jumping rope, and lifting weights are examples.
Along with a decline in physical activity, an increase in overweight and obese older adults has been documented over the past 15 to 20 years. An age-associated reduction in size and weight of various organs has been identified, especially of the liver, lungs, and kidneys (McCance et al., 2015).
For each of the symptoms or conditions discussed in this section, topics to include in the history of the present illness are listed. Responses to questions about these topics provide clues for focusing the physical examination and developing an appropriate diagnostic evaluation. Questions regarding medication use (prescription and over-the-counter preparations) as well as complementary and alternative therapies are relevant for each area.
Compared with usual weight; time period (sudden, gradual); intentional or unintentional
Desired weight loss: eating pattern, diet plan used, food preparation, food group avoidance, average daily calorie intake, appetite, exercise pattern, support group participation, weight goal
Undesired weight loss: anorexia; vomiting or diarrhea, difficulty swallowing, other illness symptoms, time period; frequent urination, excessive thirst; change in lifestyle, activity, mood, and stress level
Preoccupation with body weight or body shape: never feeling thin enough, fasting, unusually strict caloric intake; unusual food restrictions or cravings; laxative abuse, induced vomiting; amenorrhea; excessive exercise; mood, stress level; alcohol intake
Medications: chemotherapy, diuretics, insulin, fluoxetine, prescription and nonprescription appetite suppressants, laxatives, oral hypoglycemics, steroids, herbal supplements
Total weight gained: time period, sudden or gradual, desired or undesired, possibility of pregnancy
Change in lifestyle: change in social aspects of eating; more meals eaten out of the home; meals eaten quickly and “on the go”; change in meal preparation patterns; change in exercise patterns, mood, stress level, or alcohol intake
Medications: steroids, oral contraceptives, antidepressants, insulin
Coarsening of facial features, enlargement of hands and feet, moon facies
Change in fat distribution: trunk versus generalized
Infancy, prematurity, congenital heart disease
Fever, infection, burns, trauma, pregnancy, hyperthyroidism, cancer, athlete
External losses (e.g., fistulas, wounds, abscesses, chronic blood loss, chronic dialysis)
Chronic illness: liver disease, celiac disease, inflammatory bowel disease, surgical resection of the gastrointestinal tract, diabetes, congestive heart failure, hypothyroidism, hyperthyroidism, pancreatic insufficiency, chronic infection (e.g., human immunodeficiency virus [HIV] and tuberculosis), or allergies
Previous weight loss or gain efforts: maximum body weight, minimum weight as an adult
Previously diagnosed eating disorder, hypoglycemia
Obesity, dyslipidemia ( Box 8.2 )
In the United States just over one-third of adults older than 20 years are obese and an additional one-third are overweight. Poor diet and physical inactivity (regardless of weight status) are associated with serious chronic diseases including type 2 diabetes, hypertension, cardiovascular disease, osteoporosis, and some types of cancer.
About half of American adults (117 million individuals) have one or more preventable chronic diseases related to poor diet and physical inactivity.
More than 29 million U.S. adults (9.3% of the U.S. population) have diabetes. Over 90% of these individuals have type 2 diabetes. An additional 86 million adults have prediabetes.
Cardiovascular disease (coronary heart disease, stroke, hypertension, and high total blood cholesterol) affected 35% of the U.S. population in 2010. About 610,000 Americans die from heart disease each year; 73.5 million adults have high low-density lipoprotein (LDL). About 75 million adults have hypertension and an additional third have prehypertension.
Cancers linked to poor diet include breast (postmenopausal), endometrial, colon, kidney, gallbladder, and liver.
The Division of Nutrition, Physical Activity, and Obesity at the Centers for Disease Control and Prevention has a wealth of information and useful resources for patients and healthcare professionals ( www.cdc.gov/nccdphp/dnpao/index.html ).
Constitutionally short or tall stature, precocious or delayed puberty
Genetic or metabolic disorder: diabetes (see list of chronic illnesses under Past Medical History)
Eating disorder: anorexia, bulimia
Alcohol use disorder
Nutrition: appetite; usual calorie intake; vegetarianism; medical nutrition therapy guidelines followed; religious/cultural food practices; proportion of fat, protein, carbohydrate in the diet; intake of major vitamins and minerals (e.g., vitamins A, C, and D; iron; calcium; folate)
Use of vitamin, mineral, and herbal supplements
Usual weight and height; current weight and height; ability to maintain weight, goal weight
Use of alcohol
Use of illicit drugs
Food insecurity (i.e., limited or uncertain availability of nutritionally adequate and safe foods); limited/fixed income; eligibility for the Supplemental Nutrition Assistance Program (SNAP; formerly the Food Stamp Program); financial and psychosocial stressors
Functional assessment (i.e., ability to shop and prepare foods); access to healthy foods in their neighborhood; access to food storage/preparation equipment (refrigerator, stove, oven)
Typical mealtime situations, companions, living environment
Use of oral supplements, tube feedings, parenteral nutrition
Dentition: dentures, missing teeth, gum disease
Estimated gestational age, birth weight, length, head circumference
Following an established percentile growth curve
Unexplained changes in length, weight, or head circumference
Poor growth/failure to thrive: falling one or more standard deviations off growth curve pattern; below the fifth percentile for weight and height; infant small for gestational age; quality of parent-infant bond and interaction; psychosocial stressors and food insecurity
Rapid weight gain: overfeeding
Nutrition: breastfeeding frequency and duration; type and amount of infant formula; method of formula preparation; time it takes to drink one feeding; intake of protein, calories, vitamins, and minerals adequate for growth; vegetarianism; cow’s milk protein and other food allergies; vitamin and mineral supplements; number of fast food meals eaten per week; eligibility for Women, Infants, and Children (WIC) program or school breakfast and lunch programs
Hours of screen time per day (i.e., television, computer use, video and electronic games); access to safe areas for physical activity
Chronic illness: cystic fibrosis, phenylketonuria (PKU), celiac disease, inborn errors of carbohydrate metabolism, amino acid and fatty acid oxidation disorders, tyrosinemia, homocystinuria, Prader-Willi syndrome
Development: achieving milestones at appropriate ages
Congenital anomalies, prematurity, prolonged neonatal hospitalization, cleft palate, malformed palate, tongue thrust, feeding and swallowing disorders, prolonged enteral tube feeding (gastrostomy and gastrojejunostomy), gastroesophageal reflux, malabsorption syndrome or chronic diarrhea, formula intolerance, neurologic disorders, congenital heart disease, others
Initiation of sexual maturation of females: early (before 7 years) or delayed (beyond 13 years); signs of breast development and pubic hair, age at menarche
Initiation of sexual maturation of males: early (before 9 years) or delayed (beyond 14 years); signs of genital development and pubic hair
Short stature: not growing as fast as peers, change in shoe and clothing size in the past year, extremities short or long for the size of the trunk, height of parents, size of head disproportionate to the body
Tall stature: height of parents, growing faster than peers, signs of early sexual maturation
Nutrition: intake of protein, calories, vitamins, and minerals adequate for growth; vegetarianism; number of fast food meals eaten per week; food allergies; vitamin and mineral supplements; herbal supplements; appetite suppressants; laxative use; alcohol use
Preoccupation with weight; overly concerned with developing muscle mass, losing body fat; excessive exercise; weighs self daily, boasts about weight loss, weight goals; omits perceived fattening foods and food groups from the diet
Risk factors for eating disorders
Weight preoccupation
Poor self-esteem, perfectionist personality
Self-image perceptual disturbances
Chronic medical illness (insulin-dependent diabetes)
Family history of eating disorders, obesity, alcohol use disorder, or affective disorders
Cultural pressure for thinness or outstanding performance
Athlete driven to excel (e.g., gymnasts, ice-skaters, dancers, boxers, and wrestlers)
Food cravings, restrictions
Compulsive/binge eating
Difficulties with communication and conflict resolution; separation from family
Use of appetite suppressants and/or laxatives
Chronic disease, such as inflammatory bowel disease, cystic fibrosis, malignancy
Medications: steroids, growth hormones, anabolic steroids
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