KNH 411
1
 Intake
 Measured in kilojoules (kJ) or kilocalories (kcal) - food
energy
 Determined by bomb calorimeter
 Nutrition Facts label, food composition tables, dietary
analysis software
 KJ: amount of work to move 1 kilo for 1 m with the force
of 1 Newton
 Kcals: amount of heat to raise 1 L of water by 1 degree
Celsius
 CHO: 4 kcals/gram or 17 KJ/gram
 Pro: 4 kcals/gram or 17 KJ/gram
 Fat: 9 kcals/gram or 38 KJ/gram
 Alcohol: 7 kcals/gram or 29 JK/gram
 24-Hour Energy Expenditure (EE) (total amount of
energy expended in 1 day)
 Resting energy expenditure (REE)
 60-75%
 Amount energy needed for heart, lungs, brain, liver, and
kidneys to function
 Thermic effect of food
 Physical activity
 Most variable
 ~23%
 Resting energy expenditure (REE)
 Able to sustain life, keep vital organs functioning
 60-75% of EE, 1 kcal/kg body wt./hr
 factors affecting REE:
 Lean body mass: (more metabolically active than adipose tissue, so higher
amount uses more REE; males generally have a greater % than women
 Male sex
 Body temperature: can raise with exercise; clinical setting: fever
 Age: 2% decrease every decade after 30 b/c decrease lean muscle mass with
age
 Energy restriction: decrease REE—plateau effect
 **Genetics: can inherit and higher or lower REE
 Basal energy expenditure (BEE)
 Difficult to measure
 Measured in the AM when the subject is without food
for at least 12 hours; have to be in a neutral
environment and laying down—a much more accurate
number
 10-20% lower than
 Thermic effect of food (TEF)
 Measured for several hours postprandial
 Cost to digest, absorb, metabolize, store, and eliminate
nutrients
 10% of EE (with mixed diet of CHO, Pro, Fat
 Specific Dynamic Action of Food= another name for TEF
 Large amount of food would raise TEF
 Fat has lowest TEF
 Protein has the highest TEF (b/c of cost of processing amino
acids
 Peaks 1 hour after food and can last 4-6 hours
 Physical Activity EE
 Most variable
 20-25% of EE
 Influenced by 1. body weight, 2. number of muscle groups
used, 3. intensity, 4. duration and 5. frequency of activity
 Active athletes/people who do heavy labor (lumber
jack)=can have 1.5 x’s 25%
 Why do heavy weight people expend for energy? True labor
of carrying a lot of weight around
 Methods
 Equations (we rely on heavily in classroom settings)
 Should account for gender, age, weight, stature, and physical
activity
 Indirect calorimetry
 More accurate measurement
 Used in ICU setting w/ critically ill patients
 Doubly-labeled water
 Mostly used in human research facilities
 Direct calorimetry
 Not many places have the resources for this
 Equations for estimating EE
 Harris-Benedict
 Uses indirect calorimetry
 WHO-developed in 1980s
 Not stature addressed (didn’t think height would have a good
predictive advantage)
 IOM DRI – estimated energy requirement (EER)
 Includes physical activity (PA) coefficient
 Separate calculations for overweight adults and overweight
children and adolescents – based on BMI
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
 Indirect Calorimetry
 Metabolic research or critically ill patients
 Measures inspired and expired air by minute ventilation
 EE proportional to oxygen consumption and carbon dioxide
production
 Most commonly used method for ICU settings (best method)
 More accurate than formulas Harris-Benedict/Mifflin St. Jeor
 Brought to bedside of patient
 Measured body energy expenditure
 Doubly Labeled Water
 “Gold standard”
 2 stable isotope forms of water
 Rate at which isotopes disappear is measured in urine over
2-week period
 More difficult/complex way to measure
 Used more in research settings
 Accurate within 1-2%
 Direct Calorimetry
 Chamber which measures heat expired through evaporation,
convection (heat transfer), and radiation
 Rarely available
 Even more complex
 Interaction of nervous and endocrine systems
 Orexigenic (stimulates appetite; associated with anti-psych
drugs; may cause you to gain weight/appetite based on
type of drug)
 Anorexigenic (stimuli that’s stressed-related; anti-anxiety;
causes weight loss; Adderall)
 Adaptive thermogenesis (thermic effect of foods; anything
regulating response to change in temperature of diet;
extreme cold/hot may alter caloric needs)
 Appetite stimulated by hypothalamus
 Secretions of pancreatic and GI hormones
 Increase and decrease appetite and food intake
 Pradar-Willi syndrome (genetic disorder)
 Hormones affecting appetite & food intake
 Insulin (high levels=decreased appetite to meet glucose)
 Glucagon (during fasting beta cells release this=decreases
appetite)
 Amylin (decreases appetite)
 Cholecystokinin (CCK) (hormone decreasing appetite)
 Glucagon like peptide-1 (hormone decreasing appetite)
 Peptide YY (hormone decreasing appetite)
 Ghrelin (stimulates appetite; Preytor Willi)
 Adipocyte – fat cell; mostly TG (in connective tissue
around the organs)
 Storage site - 90% energy reserves is TG
 Other functions (infants: maintaining body temperature)
 White fat (WAT; storage of TG from diet fat; synthesized
from CHO and fat) vs. brown fat (BAT; found in fetus,
infants, children=6%; body temp/insulation; decreases
with age and will convert to white fat)
 Lipogenesis (need to store excessive energy)
© 2007 Thomson - Wadsworth
 Adiponectin (stimulate/signals body to store fat) and leptin
(signaling that there is ample fat and body doesn’t need to store
more)
 Hypertrophy (occurs when someone is overweight—BMI 25-29);
adipose tissue mass that increases & accumulates more TG; energy
intake exceeds energy expenditure) and Hyperplasia (adipose cells
increase in number of cells can no longer lose these cells, can only
shrink them; occurs when extreme obesity—BMI >40)
 “Adiposity rebound”
 One key concern in U.S. today
 From ages 1-6, there was a change in body % fat to leaner
muscle mass, but now we are seeing that % body fat is
beginning to increase at this age up to age 8, thus these
individuals are at higher risk for a higher BMI
 “Two compartment model” – fat vs. fat-free mass
 Adipose tissue vs. Lean tissue
 Different ways to measure this: 1. skin-fold measurements,
2. underwater weighing, 3. biochemical impendents
 Use of height and weight – BMI commonly used to assess
obesity
 Does not directly measure fatness
 Clinical judgment should be used (who’s conducting
measurements)
 Body Mass Index (BMI)
 Obese ≥ 30
calculation and classifications
 BMI percentiles
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CDC growth charts
Pediatric population
≥ 95%th percentile = obesity
≥ 85%th percentile = overweight
 Important predictor of health status
 Abdominal/central body fat
 Apple, android
 Associated with obesity risk & more health concerns
related to diabetes & CVD
 Lower body fat
 Hips and thighs, pear, gynoid
 Measured by waist circumference and waist-to-hip
ratio
 Anything greater than 1 is a concern b/c related to being
fat and unhealthy
 Waist circumference
 Increased risk of type 2 DM, htn., dyslipidemia, CHD,
metabolic syndrome
 > 40 in. males, > 35 in. females – “high risk”
 Waist-to-hip ratio (WHR)
 Waist circumference/hip circumference
 Disease risk increases with WHR > 0.95 (just use 1) in
males and >0.8 in females
 Key concept: fat deep within abdomen and around
intestines and liver increases disease risk
 “Globesity,” “epidemic”
 Concern of the decade according to WHO
 In the U.S. - NHANES data--looking at overweight and obese
individuals
 Significant increases
 Canada
 36% obese
 23% overweight
 Europe
 45-80% of population
 By race, ethnicity, SES, age
 African American females (50% obese), African American males
(30% obese)
 “The age of caloric anxiety”
 Type 2 diabetes (2x’s more prevalent in obese
population)
 High blood pressure (3x’s more prevalent in obese)
 CHD (2x’s-3x’s more likely if obese)
 Cancer (esophagus, colon, rectum, pancreas, liver,
prostate)
 Mortality (doubled with increased body weight)
 Chronic energy intake exceeding energy expenditure
 Key contributors:
 Medical disorders and treatment (ex: pushing syndrome,
hyperthyroidism, of concern when see different types of
drugs being used by patients)
 Genetics (small component)
 Obesigenic environment (#1 contributor!)
 Medical disorders and treatment
Cushings syndrome, hypothyroidism, Prader-Willi
Pharmacological agents (types of drugs used by patients)
Smoking cessation (20-30 lb weight gain over decades)
Night eating syndrome (25% calories eaten at night without
even knowing it)
 Binge eating (10-25% of daily calories eaten in one sitting)
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 Genetics
 40-50% of BMI explained by genetics
 Influences taste, appetite, intake, expenditure, NEAT, storage
 More are more prone to obesity through genetics
 Environment is main reason
 “Set-point” theory—reasons why people might be gaining weight
quickly
 Multiple genes –may cause people to increase intake significantly
 Predictive in families – parents & twins
 80% of offspring with 2 obese parents
 40% of offspring with 1 obese parent
 MZ (monozygote) twins more likely than DZ (fraternal) twins
 Adopted twins: BMI correlated strongly with real parents and
not the adopted parents)
 Obese really is a mixture of genetic & environment
 Obesigenic environment
 “Toxic food environment” – convenient availability of lowcost, tasty, energy-dense foods in large portions
 Evidence supports low-energy-dense foods for satiety
 Soups, fruits, vegetables, cooked whole grains
 Barriers – cost and convenience
 Two-step process to look at and treat weight
 Willingness to change?
 Evaluate exercise as well as dietary habits
 Assessment
 BMI, waist measurements, waste-hip ratios
 Management
NIH algorithm for treatment
© 2007 Thomson - Wadsworth
 Assessment
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BMI & waist circumference
Current chronic diseases
Diet and physical activity habits
Patient’s readiness to lose weight
Identify and address barriers, coping skills, self-efficacy
Behavioral assessment (what events led them to seek
weight loss, what are there stress levels/moods related to
food)
 Management
 Use of recommended therapies
 Long-term program
 Control of factors known to increase risk of morbidity
 Therapies include – diet, physical activity, behavioral
therapy, bariatric surgery, pharmacologic treatment
 Lose 10% in 6 mo. (~1-2 lbs per week)
 Nutrition therapy
Reduce intake 500-1000 kcal/d.
Lose 1-2 lbs./week
NIH low-kcalorie diet
Minimize CVD risk factors – NCEP Therapeutic Lifestyle
Changes diet
 1000-1200 kcal/d women, 1200-1600 kcal/d men minimum
 Unclear whether altering macronutrient levels is beneficial
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© 2007 Thomson - Wadsworth
 Physical Activity
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Crucial for weight maintenance
Minimum 30-45 min moderate activity 3-5 days/week
Initiate slowly and gradually
Can be programmed or lifestyle activities
 Behavior Therapy
 Techniques for identifying and overcoming barriers
 Self-monitoring
 Stimulus control
 Rewards
 Pharmacologic Treatment
 BMI ≥ 30 or ≥ 27 with risk factors
 Consider cost and side effects, and rebound weight gain
 Long-term use
 Sibutramine (Meridia)
 Orlistat (Xenical)
 Others for short-term use
 Surgery
 Bariatric surgery – BMI ≥ 40 or ≥ 35 with risk factors
 Roux-en Y gastric bypass, vertical banded gastroplasty,
adjustable band gastroplasty
 Assess benefits vs. risks
 Preoperative screening & education important