NUTR 442
Nutrition Assessment Laboratory
Spring 2008
(under construction)
David L. Gee, PhD
Professor and Program Director
of Food Science and
Nutrition
NUTR 442
Nutrition Assessment Laboratory
Spring 2008
(under construction)
David L. Gee, PhD
Professor and Program Director
of Food Science and
Nutrition
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NUTR 442 - NUTRITION ASSESSMENT LABORATORY
Instructor: David Gee, PhD
Office: 109 PE Building
Office Hours : TuTh 9-10AM, MW 10-11AM or by appointment (963-2772,
geed@cwu.edu)
Lecture: Tue (Thur) 2-2:50
Lab: Sec .02: Tue 3-4:50
Sec .03: Thur 2-3:50
Sec
.04: Wed 3-4:50
COURSE DESCRIPTION: Overview of current tools for nutritional assessment with laboratory experience.
STUDENT OUTCOMES:
1. Student will develop a basic understanding of the scientific
principles of the various methods of nutritional assessment.
2. Student will understand the advantages, limitations, and applicability
of the various methods.
3. Student will be able to apply the tools of nutritional assessment
to clinical cases including it's use in the planning, intervention, and
evaluation of patient care.
REQUIRED TEXTBOOK:
Nutritional Assessment. 3rd ed. R. Lee & D. Nieman.
2003.
New Required Fee
Although all materials used for this laboratory course has been covered within
the department budget, the Student Health Center initiated a blood collection
fee beginning in 2007 for all CWU courses requiring a blood draw. When you
go to the Student Health Center your student account will be charged $10 at that
time. If you have never used the services at the Student Health Center,
you will need to arrive 15 minutes prior to your appointment to fill out the
necessary paperwork.
| Laboratory Reports
7 reports, 20 points each |
140 points |
| Exam 1 (May 1) | 100 points |
| Final Exam (Tuesday, June 5, 2PM-4PM) | 100 points |
| TOTAL | 340 points |
(full attendance is expected; missing a lab will result in a deduction
of 10 points from the laboratory report (if turned in). Laboratory reports
are due at the beginning of the following lab period. A 10% deduction
will be made for every day the report is late.
| Grading Scale | Letter Grade |
| 90-100% | A, A- |
| 80-89% | B+, B, B- |
| 65-79% | C+, C, C- |
| 55-64% | D+, D, D- |
Laboratory
Report Format
The format of the laboratory reports in FCSN 442 will give the students
the opportunity to present their findings using the SOAP format that is
commonly used in clinical settings. Typically, SOAP notes are written
in a very cryptic/abbreviated form in order for both the writer and reader
to save time. In this class, your SOAP notes will be brief but written
in a narrative form with complete sentences. Your laboratory reports
are required to be typed, except for calculations. These calculations
should be hand written (but neat) and be on separate attached pages.
Most of you will use the same subjects for each weeks laboratory.
You may wish to keep adding to your SOAP notes every week so that your
assessment and plan builds on the growing amount of data you are collecting
for each subject. If you do your reports this way, please use bold
or italics to indicate all new information for that week.
Title
Objective(s) of Experiment for that week
SOAP notes on each subject
Subjective: Pertinent information obtained from patient or patient’s family or significant other. The subjective data expresses the patient’s perception of a problem.
Objective: Factual information relevant to the problem that can be confirmed by others. This section includes laboratory values, physical findings and observations by health professionals. Factual nutrition information found in this section could include dietary intake, anthropometric information, calculations of nutrient needs, and observed difficulties in eating.
Assessment: The health care provider's evaluation or interpretation of the subjective and objective data. The health care provider uses his/her professional judgment about a certain problem.
Plan: The specific course of action to be taken based
on the subjective and objective data as well as the assessment made.
The plan may include any further workup needed (additional tests), therapy
(suggested dietary changes), and patient education.
Nutrition Assessment
David L. Gee, PhD
FCSN 442 - Nutrition Assessment Laboratory
Definition of Nutritional Assessment (US DHHS)
The measurement of indicators of:
dietary status
nutrition-related health status
Purpose:
identify possible occurrence, nature, and extent of impaired nutritional
status
Opportunities for Nutrition Assessment
Prevention of Chronic Diseases
Coronary Heart Disease
Dietary Assessment
Obesity
Blood Pressure
LDL-cholesterol, HDL-cholesterol
BMI, fat distribution
Opportunities for Nutrition Assessment
Prevention of Chronic Disease
Hypertension
Dietary Assessment
Body Mass Index, fat distribution
Blood Pressure
Opportunities for Nutrition Assessment
Prevention/treatment of chronic diseases
Diabetes Mellitus
fasting blood glucose
glucose tolerance test
dietary assessment
BMI, fat distribution
Opportunities for Nutrition Assessment
Improve outcome of pregnancy
low birthweight babies
reduce birth defects
dietary assessment
weight gain during pregnancy
Opportunities for Nutrition Assessment
Improved health of infants and children
height and weight
dietary assessment
Opportunities for Nutrition Assessment
Protein Calorie Malnutrition in Hospitalized Patients
Incidence of PCM
1988 DeHoog
UW hospital
based on albumin and body weight
1979: 33% at nutritional risk
1985: 40% at nutritional risk
1987: 43% at nutritional risk
Protein Calorie Malnutrition in Hospitalized Patients
JADA 1993
228 pts @ U. Alabama Hospital
compared to 1976 findings
Likelihood Of Malnutrition Score (LOM)
serum folate & ascorbate
weight & height
tricep skinfold (TSF)
midarm muscle circumference (MAMC)
total lympocyte count (TLC)
albumin
hematocrit (hct)
Effect of PCM on Hospitalized Patients
slow wound healing
increased incidence of infections
increased incidence of complications
increased mortality rate
compromised medical therapies
Causes of PCM: Inadequate nutrient intake
loss of appetite
poor food choices
poverty
isolation
chemical abuse
GI pain/discomfort
Causes of PCM: Malabsorption of nutrients
Pancreatic/biliary diseases
intestinal inflammatory diseases
parasites
side effect of therapy
drugs
radiation
Causes of PCM: Increased nutrient losses
diarrhea
unusual urinary losses
glucouria
proteinuria
vomiting
thermal burns
Causes of PCM: Increased nutrient requirement
Fever
Catabolic Stress Response
trauma
burns
infections
cancer
Nutritional Assessment Methods
Dietary Methods
survey quantity of food consumed over time
assessing pattern of typical food use over previous several months
Anthropometric Methods
measurements of physical dimensions and composition of the body
Nutritional Assessment Methods
Laboratory Methods
measurement of chemical in blood, urine, tissue that have a relationship
to nutritional status
Clinical Methods
medical history & physical examination
signs & symptoms of malnutrition
Applications
Assess energy status
under nourished
over nourished
Assess protein status
Assess changes due to disease or therapy
Assessment of Stature (Height)
Adults
weight for height
Children
height for age
weight for height
Assessment of Stature (Height)
Methodology
Stadiometer
bare feet
body & head position
avoid parallax error
Indirect measurement of height
When is it appropriate?
Stature from arm span
Stature based on knee height
Assessment of Body Weight
Metropolitan Life Insurance Tables
1959 Build Study
5 million policy holders
20% ht & wt self reported
followed for 20 yrs
mortality risk
weight with clothing (4-7 lbs)
height with shoes (1-2 inches)
1983 Metropolitan Life Tables
4 million policy holders
10% data self reported
weight with clothing (3-5 lbs)
height with shoes (1 inch)
WLM lower in 1983, particularly with shorter females
smoking effect?
Determination of Frame Size
Elbow breadth
Height to Wrist Circumference Ratio
discrepancy between methods
Weight Adjustments for Amputations
Foot 1.8%
below knee 6%
above knee 15%
entire leg 18.5%
hand 1%
below elbow 3%
entire arm 6.5%
Body Mass Index
BMI = BW(kg)/H2(m2)
Higher correlation with health risks and mortality than weight for
height
USDA Dietary Guidelines for Healthy Weight
NIH Clinical Guidelines
Body Mass Index
Calculate target weight from BMI
target BW = target BMI x H2
5’10” = 1.78m
H2 = 3.16
target BMI = 25
target BW = 25 x 3.16 = 79kg = 174 lbs
Assessment of Body Fat Distribution
Waist to Hip Ratio
>0.9 males, >0.8 females
based on age and gender
Waist Circumference
males > 40 inches
females > 35 inches
Significance of Weight Loss Due to Illness
% wt change = (usual BW- current BW) x 100
usual BW
At risk if:
> 5% loss in one month
>10% loss in 6 months
Assessment of Body Composition
Body Composition Analysis vs. Body Weight Assessment
Advantages
Direct assessment of body fatness
athletes
inadequate stores in patients
Monitor changes
weight loss
effect of medical therapy
Body Composition Analysis vs. Body Weight Assessment
Disadvantages
limited database
false assumption in all field methods
errors by technicians
limited understanding by clients
Models of body composition
2 compartment models
Fat mass and Fat-free mass
Fat mass and Lean body mass
assessment methods using this model
skinfold thickness
hydrodensitometry
bioelectric impedance
Models of body composition
4 compartment models
water, protein, fat , minerals
isotope dilution
dual emmision x-ray absorptiometry (DEXA)
computed tomography (CT, CAT)
Skinfold Thickness
measures double thickness of skin and subcutaneous fat
Advantages:
inexpensive
fast
portable
large database
Skinfold Thickness
Assumptions:
about 50% of fat is subcutaneous
good predictor of non-subcutaneous fat
sites selected represent average thickness of all subcutaneous fat
compressibility of fat similar between subjects
thickness of skin negligible
Skinfold Thickness
Limitations
Technician error
exercise increases skin thickness
dehydration reduces skin thickness
edema increases skin thickness
dermatitis increases skin thickness
Single Site Measurements
Tricep skinfold thickness
Subscapular skinfold thickness
not for estimating body fat determination
for comparing against other reference data
appendix O (p633-636) (TSF)
appendix P (p637-640) (SSF)
Two site measurements
Tricep SF and Subscapular SF
correlated with body fatness in children
fig. 6-33 (p259)
Tricep SF and calf SF
fig. 6-34 (p 260)
Multiple Site Measurements
many sites
many equations
table 6-10 (p261) Jackson & Pollock
table 6-11 (p261) Durnin & Womersley
density and %body fat (Siri)
% BF = (495/BD) - 450
note error in text w/ Brozek (p260)
Circumference Measurements
Principle of: measure two “fat” sites and one “muscle site” to
estimate fat and lean body mass.
Very limited database
Easy to do
Hydrodensitometry
Principle:
two compartment model
density related to relative amounts of two compartments
D(fat) = 0.90 g/ml
D(lbm) = 1.10 g/ml
D(water) = 1.00 g/ml
Hydrodensitometry
Density = Body weight/Body volume
estimation of body volume
Archimedes principles:
volume of submerged object = volume of water displaced
weight in air - weight underwater = weight of water displaced
Hydrodensitometry
wt of water displaced = vol of water displaced
= vol of body (BV)
therefore: BW-UBW = BV
BD = BW / BV
calculate %BF from BD
Hydrodensitometry: Assumptions
Density of fat and lean tissues are constants
bone density differences
muscle density differences
hydration status effects
GI gas volume is constant
Hydrodensitometry: Limitations
Measurement of residual volume
Precision of underwater weight
Cost
Non-portable
Limit types of subjects
Whole Body Pethysmography
Measures body volume by measure air displacement
Actually measures pressure changes with injection of known volume of
air into closed chamber.
Large body volume reduces air volume in chamber and results in bigger
increases in pressure following injection of known volume of air.
Whole Body Pethysmography
Advantages over hydrodensitometry
subject acceptability
more consistent
residual volume not a factor
Limitations
costs: $25 - 30K
assumes constant density of lean and fat tissue
Bioelectrical Impedance Analysis
1994 NIH Technology Assessment Conference
“BIA provides a reliable estimate of total body water under most conditions.”
“It can be a useful technique for body composition assessment in healthy
individuals”
Bioelectrical Impedance Analysis
BIA measures impedance by body tissues to the flow of a small (<1mA)
alternating electrical current (50kHz)
Impedance is a function of:
electrical resistance of tissue
electrical capacitance (storage) of tissue (reactance)
BIA: basic theory
The body can be considered to be a series of cylinders.
Resistance is proportional to the length of the cylinder
Resistance is inversely proportional to the cross-sectional area
BIA: basic theory
Volume is equal to length of the cylinder times its area
Therefore, knowing the resistance and the length, one can calculate volume.
Assuming that the current flows thru the path of least resistance (water) , then the volume determined is that of body water.
BIA: basic theory
Assume fat free mass has a constant proportion of water (about 73%)
Then calculate fat free mass from body water
Assume BW = FFM + FM
Then calculate fat mass and %body fat
NHANES III BIA Equations
Males
FFM = -10.68 + 0.65H2/R + 0.26W + 0.02R
Females
FFM = -9.53 + 0.69H2/R + 0.17W + 0.02R
Where
FFM = fat free mass (kg)
H = height (cm)
W = body weight (kg)
R – resistance (ohms)
% BF = 100 x (BW-FFM)/BW
BIA Calculations
DATA
R = 520 ohms
BW = 170 lbs = 77.3 kg
H = 70” = 178 cm
CALCULATIONS
FFM = -10.68+(0.65H2/R)+0.26W+0.02R
FFM = -10.68+(0.65x1782/520)+0.26(77.3)+0.02(520)
FFM = -10.6 + 39.6 + 20.1 + 10.4 = 59.5 kg
FM = W – FFM = 77.3 – 59.5 = 17.8 kg
%BF = (17.8/77.3)x100 = 23%
BIA: Advantages and Limitations
Advantages
costs ($500-$2000)
portable
non-invasive
fast
Limitations
accuracy and precision
no better/worse than hydrodensitometry
Major types of BIA analyzers
BIA Protocol
Very sensitive to changes in body water
normal hydration
caffeine, dehydration, exercise, edema, fed/fasted
Sensitive to body temperature
Avoid exercise
Sensitive to placement of electrodes
conductor length vs. height
Body Composition Data NHANES III – 1988-1994
All adults > 19 yrs
Mean % Body Fat
Men: 21.9% + 11.6% (SD)
Women: 32.4% + 17.8%
Mean BMI
Men: 26.5 + 7.8
Women: 26.4 + 11.7
Mean waist circumference
Men: 95.1 + 18.6 cm (cutpoint > 101.6 cm)
Women: 88.6 + 30.2 cm (> 89 cm)
Body Composition Data NHANES III – 1988-1994
Adults with BMI = 18.5-25
Mean % Body Fat
Men: 17.6% + 7.8% (SD)
Women: 26.7% + 8.9%
Mean BMI
Men: 22.7 + 3.2
Women: 22.0 + 2.2
Mean waist circumference
Men: 84.7 + 8.9 cm (cutpoint > 101.6 cm)
Women: 78.0 + 13.4 cm (> 89 cm)
Assessment of Protein
Status
FCSN 442 - Nutrition Assessment Laboratory
Dr. David L. Gee
Central Washington University
Assessment of Protein Status
Anthropometric Assessment
BMI, body composition estimations
midarm muscle circumference/area
Laboratory Assessment
serum albumin
other serum proteins (transferrin, prealbumin, retinol-binding protein)
urinary creatinine excretion
total lymphocyte count
Midarm Muscle Area
Estimate of MAMA is an estimate of overall muscle mass
single point vs serial measurments
Assumptions
arm, muscle, bone are circular
TSF is 2X the thickness of fat
bone area is constant
Midarm Muscle Circumference
MAMC = AC - (.314 x TSF)
MAMC = midarm muscle circumference in cm2
AC = arm circumference in cm
TSF = tricep skinfold in mm
Mid Arm Muscle Area
MAMA = ((AC - (3.14 x TSF)2 ) / (4 x 3.14)
MAMA = midarm muscle area (cm2)
AC = arm circumference (cm)
TSF = tricep skinfold thickness (cm)
adjusted MAMA
corrected for “bone free” MAMA
p-304
Serum Albumin
Major serum protein
Synthesized in liver
Maintains serum osmolarity
Serum carrier of small molecues
Most common indicator of depleted protein status
Serum Albumin
Half life = 14-20 days
large body pool
poor indicator of early protein depletion and repletion
Levels affected by rate of synthesis (liver disease)
Serum Albumin
Levels affected by abnormal losses
thermal burns
nephrotic syndrome
protein-losing enteropathies
Levels affected by fluid status
congestive heart disease & fluid overload
dehydration
Serum Transferrin
Function: transport protein for iron
half-life = 8-9 days
better index of changes of protein status
Influenced by other factors
iron status
increased during pregnancy, estrogen therapy
reduced in protein-losing enteropathy, nephropathy, acute catabolic
stress
limited usefulness in protein status assess.
Serum Prealbumin
AKA transthyretin and thyroxine-binding prealbumin
functions:
transport protein for thyroxine
carrier protein for retinol binding protein
short half life (2-3d), small body pool
sensitive indicator of protein status
responds more rapidly than albumin or transferrin
Serum Prealbumin
Returns to normal at beginning of nutritional therapy
therefore do not use as endpoint for terminating nutritional therapy
Influenced by other factors
increased in chronic renal failure on dialysis
reduced in acute catabolic states, post surgery, tissue trauma, sepsis
generally considered preferable than albumin and transferrin
Retinol Binding Protein
Function: carrier for retinol
complexes with prealbumin (1:1)
responds like prealbumin
very rapid turnover (12 hours), very small body pool
may be too sensitive and complicates precise measurements
generally not considered to be more useful than prealbumin
Immunocompetence
Immune system affected by nutritional status
Tests of immunocompetence useful functional indicators of nutritional
status
Delayed Cutaneous Hypersensitivty (DCH)
intradermal injection of antigens
Total Lymphocyte Count (TLC)
Total Lympocyte Count
White blood cell count
elevated with infections
used with % lymphocyte to get total lymphocyte count (TLC)
TLC = (%lymp x WBC)x100
ex: TLC=(37.2%x4100)x100 =1525 cells/mm3
Total Lympocyte Count
Normal = 1200-1800 cells/mm3
Moderate PCM = 800-1200
Severe PCM = < 800
Urinary Creatinine Excretion
Creatinine excreted in proportion to muscle mass
LBM estimated by comparing 24-hr urine creatinine excretion with standard
based on stature or reference values of 23 and 18 mg/kg for M and F
Creatinine Height Index
CHI = (23hr urine creatinine x 100) / (expected 24hr urine creatinine
for height)
expected values in table 9-1 (p395)
CHI > 80% = normal
CHI = 60-80% = mild protein depletion
CHI = 40-60% = moderate depletion
CHI < 40% = servere depletion
Glucose
Tolerance Test: Diabetes Mellitus
Dr. David Gee
FCSN 442 - Nutrition Assessment Laboratory
Diabetes Mellitus
Hyperglycemia
Dyslipidemia
Altered protein metabolism
Prevalence
16 million Americans
50% undiagnosed
Long Term Complications
36,000 deaths/yr directly due to DM
premature coronary heart disease
blindness
renal failure
amputations
economic costs
Type 1 Diabetes Mellitus
~ 10% of diabetics
a.k.a.
Insulin Dependent DM (IDDM)
Juvenile diabetes
absolute deficiency of insulin
Type 2 Diabetes Mellitus
~ 90% of diabetics
a.k.a.
Non Insulin Dependent DM (NIDDM)
Adult onset DM
peripheral insulin resistance
Management Goals
maintain [glu] close to physiological norms
1993 Diabetes Control and Complications Trial
demonstrated benefits of glucose control
effectiveness of individualized therapy (diet, exercise, medication)
Criteria for testing for DM in assymptomatic, undiagnosed patients
> 45 yrs, every 3 yrs
< 45 yrs, every 3 yrs if:
BMI > 27
1st degree relative with DM
Blacks, Hispanic, Native American
Hx Gestational Diabetes or baby > 9 lbs
Criteria for testing for DM in assymptomatic, undiagnosed patients
< 45 yrs, every 3 yrs if:
hypertension
HDL < 35 mg/dl
TG > 250 mg/dl
previous Dx of impaired glucose tolerance or impaired fasting glucose
Fasting Blood Glucose
> 8 hr fast
DM if FBG > 126 mg/dl on 2 occasions
Impaired FBG if : 110 - 125 mg/dl
Glucose Tolerance Testing
for adults with impaired FBG
during pregnancy
procedure
Diagnostic Criteria
DM if [glu] > 200 mg/dl at 1 or 2 hours
IGT if [glu] >140 - 200 at 1 or 2 hours
normal if [glu] < 140 mg/dl
Laboratory
Values for Nutritional Assessment
David L. Gee, PhD
FCSN 442
Nutrition Assessment Laboratory
Assessment of Renal Function: Blood Urea Nitrogen
BUN
Urea: end product of amino acid metabolism
Produced in liver
Excreted by kidneys
Elevated due to renal insufficiency
BUN
Increased with dehydration
Decreased with liver disease
Unaffected by protein intake in normal subjects
Elevated by protein intake in dialysis patients
Urinary urea excretion affected by protein intake
Serum Creatinine
Endproduct of creatine metabolism
Excreted by kidneys into urine
Serum levels increased with renal insufficiency
Urinary excretion (24hr) proportional to muscle mass (note meat consumption,
creatine supplementation)
Serum Albumin
Major serum protein
Synthesized in liver
Maintains serum osmolarity
Serum carrier of small molecues
Most common indicator of depleted protein status
Serum Albumin
Half life = 14-20 days
large body pool
poor indicator of early protein depletion and repletion
Levels affected by rate of synthesis (liver disease)
Serum Albumin
Levels affected by abnormal losses
thermal burns
nephrotic syndrome
protein-losing enteropathies
Levels affected by fluid status
congestive heart disease & fluid overload
dehydration
Globulin Proteins
Water-insoluble proteins
Soluble in saline
Includes all serum proteins except albumin and prealbumin
Acute phase proteins
Other assessments of protein status
Other serum proteins
Transferrin
Prealbumin
Retinol binding protein
Immunocompetence
Total lymphocyte count
Delayed cutaneous hypersensitivity
Transferrin
Function:
serum iron transport protein made in liver
Advantages over albumin
More sensitive
Smaller body pool
Shorter half-life
Problems
Decreased with chronic infections, protein-losing enteropathies, nephropathy,
etc.
Increased with iron deficiency, pregnancy, estrogen therapy, acute
hepatitis
Prealbumin
Function
Transports thyroxine (transthyretin)
Carries retinol binding protein
Advantages over albumin
More sensitive
Small body pool, short half life
Limitations
Responds very quickly, not good for final endpoint of nutritional support
(reflects current dietary intake)
Concentrations altered in various disease states
Retinol Binding Protein
Function
Transports retinol, made in liver, carried with prealbumin
Advantages of albumin
More sensitive, small body pool, very short half-life
Limitations
Half-life shorter than prealbumin, too sensitive, reflects dietary
intake rather than protein status
Affected by disease states, decreased with vitamin A deficiency
Measures of Immunocompetence: Total Lymphocyte Count
CBC with differential count
TLC = (%lymp x WBC)/100
ex: TLC=(37.2%x4100)/100 = 1525cells/mm3
Assessment of protein status
1200-1800: mild depletion
800-1200: moderate depletion
< 800: severe depletion
TLC affected by disease states & drugs
Measures of Immunocompetence: Delayed Cutaneous Hypersensitivity
Intradermal injection of antigens
Streptokinase, candidin, trichophyton, tuberculin, mumps
Hardening (induration) and redness (erythema) noted in 24-72 hrs in
normally nourished subjects
Also affected by vitamin status, patient prior exposure, disease state,
etc..
Bilirubin
Endproduct of heme catabolism
Made in spleen, liver, bone marrow
Excreted into bile from liver
Elevated bilirubin is neurotoxic
Jaundice
Bilirubin
Indirect Bilirubin
free bilirubin (unbound)
circulating form
Direct Bilirubin
bilirubin conjugated (bound) to other compounds (glucuronic acid)
made in liver
excreted in bile
Elevated Direct Bilirubin
Post hepatic jaundice
obstruction in liver, bile duct
Elevated Indirect Bilirubin
Pre hepatic jaundice
excessive hemolysis
liver disease
hepatitis
premature infants
underdeveloped liver
Alkaline Phosphatase (ALP)
Found in liver, bone, placeta, intestine
elevated levels in diseases of these tissues
Lactate Dehydrogenase (LDH)
Found in muscle, heart, liver, pancreas, spleen, brain
Elevated in injury to these tissues
Isozymes useful in detecting MI and other specific tissue injury
Transaminases
High in liver and other tissues
Elevated in serum when tissue injured
ALT (alanine transaminase)
SGPT (serum glutamate pyruvate transaminase = ALT)
AST (aspartate transaminase)
SGOT (serum glutamate oxaloacetate transaminase = AST)
Iron Status
Stage one - iron deficiency
Depletion of iron stores
Ferritin - primary storage form of iron
Serum ferritin reflects tissue levels
Low serum ferritin - early iron deficiency
Iron Status
Stage Two Iron Deficiency
Iron deficiency without anemia
Transferrin - serum iron transport protein
Serum iron reflects transferrin iron
Each transferrin protein can bind two iron atoms
Transferrin
Normal transferrin saturation= 30%
Total Iron Binding Capacity (TIBC)
add excess iron to serum to saturate transferrin, remove unbound iron,
measure total iron = TIBC
TS = [(serum iron)/TIBC]*100
low TS = stage 2 iron deficiency
Iron Status
Stage Three Iron Deficiency
Iron deficiency anemia
low iron stores (low serum ferritin)
low transferrin saturation
microcytic hypochromic anemia
Hemoglobin
Widely used diagnosis of late stage iron deficiency
Table 9-6 cutoff values for Hgb based on 5th pct, NHANES II
hemodilution during
early pregnancy
early exercise training
Hematocrit
Packed RBC cell volume
%HCT = % of RBC making up whole blood volume
Manual measurement
Automated blood counters
calculated from RBC count and MCV
high due to dehydration
Mean Corpuscular Volume
MCV
average size of RBC
elevated with:
folate and B12 deficiency
decreased with:
iron deficiency
Mean Corpuscular Hemoglobin
MCH = amount of hemoglobin in RBC
picograms per cell
Mean corpuscular hemoglobin concentration (MCHC)
average concentration of HB in RBC
g/l
Hematology
White blood cell count
elevated with infections
used with % lymphocyte to get total lymphocyte count (TLC)
TLC = (%lymp x WBC)x100
ex: TLC=(37.2%x4100)x100
=1525 cells/mm3
TLC for assessing protein status
Normal = 1200-1800 cells/mm3
Moderate PCM = 800-1200
Severe PCM = < 800
Coronary Heart
Disease Risk Assessment
Update: Detection, Evaluation, and Treatment of High Blood Cholesterol
in Adults (ATP III)
David L. Gee, PhD
Professor of Food Science and Nutrition
Central Washington University
National Cholesterol Education Program (NCEP)
Adult Treatment Panel I (ATP I)
1988
strategy for primary prevention of CHD
established cutoff values for TC, HDL-C, LDL-C and CHD risk factors
National Cholesterol Education Program (NCEP)
Children’s Treatment Panel
1991
ATP II
1993
reaffirmed ATP I
secondary prevention of CHD
National Cholesterol Education Program (NCEP)
ATP III
May 2001
reaffirms ATP I, II
New features
primary prevention in persons with multiple risk factors
modifies lipid classifications
modifies implementation of prevention measures
Initial CHD Risk Assessment
Fasting lipoprotein profile
adults > 20 yrs old
every 5 years
TC, LDL-C, HDL-C, TG
Non-fasted blood sample
only TC and HDL-C usable
LDL-C = TC - HDL-C - (TG/5)
ATP III Classification of LDL- Cholesterol (mg/dl)
LDL Cholesterol
< 100 optimal
100-129 near/above optimal
130-159 borderline high
160-189 high
>190 very high
ATP III Classification of Total and HDL Cholesterol (mg/dl)
Total Cholesterol
<200 desirable
200-239 borderline high
>240 high
HDL Cholesterol
<40 low (bad)
>60 high(good)
Major Risk Factors that Modify LDL-Goals
Cigarette smoking
hypertension (BP>140/90 or on anti-hypertensive medication)
low HDL-C (<40mg/dl)
high HDL-C (>60mg/dl) “negative risk factor”
family history of premature CHD
1o male relative < 55yrs
1o female relative <65yrs
age
men > 45 yrs
women > 55 yrs
CHD Risk Equivalents
Have risk of major coronary event equal to that of established CHD
Other forms of atherosclerotic disease
peripheral arterial disease
abdominal aortic aneurysm
symptomatic carotid artery disease
Diabetes
Multiple risk factors that confer a 10-year risk for CHD > 20%
Estimating 10-Year CHD Risk Framingham Risk Score
Short Term Risk (10-yr) for myocardial infarction
Age
Total Cholesterol
Smoker
HDL
Systolic BP
Estimate of 10-Year Risk for Women (Framingham Point Scores)
Estimate of 10-Year Risk for Women (Framingham Point Scores)
Estimate of 10-Year Risk for Women (Framingham Point Scores)
Estimate of 10-Year Risk for Women (Framingham Point Scores)
Estimate of 10-Year Risk for Women (Framingham Point Scores)
Estimate of 10-Year Risk for Women (Framingham Point Scores)
Estimate of 10-Year Risk for Women (Framingham Point Scores)
Spreadsheet for determining Framingham 10-yr risk.
Downloadable at:
http://hin.nhlbi.nih.gov/atpiii/riskcalc.htm
Palm III Operating System download at:
http://hin.nhlbi.nih.gov/atpiii/atp3palm.htm
includes other information from ATP III
Categories of Risk that Modify LDL-C Goals
LDL Cholesterol Goals and Cutpoints for Therapeutic Lifestyle Changes (TLC) and Drug Therapy in Different Risk Categories
Therapeutic Lifestyle Changes in LDL-lowering Therapy
TLC Diet
Therapeutic options to lower LDL-C
plant stanols/sterols (2g/d)
viscous soluble fiber (10-25 g/d)
Weight reduction
Increase physical activity
TLC diet
SFA: < 7% of Calories
PUFA: up to 10% of Calories
MUFA: up to 20% of Calories
Total Fat: 25-35% of Calories
CHO: 50-60% of Calories
fiber: 20-30g/d
Cholesterol: < 200mg/d
A Model of Steps in Therapeutic Lifestyle Changes (TLC)
Beyond LDL Lowering: Metabolic Syndrome as a Secondary Target of
Therapy
Cluster of risk factors
Associated with insulin resistance
Enhance risk of CHD at any LDL-C level
Diagnosis of Metabolic Syndrome
Three or more of the following:
Abdominal Obesity
men > 40” waist circumference
women > 35” waist circumference
Hypertriglyceridemia (>150 mg/dl)
Low HDL
men < 40 mg/dl
women < 50 mg/dl
Hypertension (>130/>85 mmHg)
Hyperglycemia (> 110 mg/dl)
Prevalence of the Metabolic Syndrome Among US Adults JAMA 287:356-359
(2002)
NHANES III (8814 adults)
Prevalence
23.7% of adult population
47 million Americans
increases with age
6.7% of 20-29 yr olds
43.5% of 60-69 yr olds
overall, prevalence similar in men and women
African-American women 57% higher
Mexican-American women 26% higher
Management of Metabolic Syndrome
Control LDL-cholesterol
Weight Control
enhances LDL-C lowering
reduces all risk factors of metabolic syndrome
Physical Activity
reduces VLDL-TG
increases HDL-C
lowers LDL-C
lowers BP
reduces insulin resistance
ATP III Guidelines - Application
Step 1
Determine lipoprotein levels from fasted blood sample
LDL-cholesterol
primary target of therapy
Total cholesterol
HDL-cholesterol
ATP III Guidelines - Application
Step 2
Identify presence of clinical atherosclerotic disease that confer high
risk
Clinical CHD
CHD risk equivalents
ATP III Guidelines - Application
Step 3
Determine presence of major risk factors (other than LDL)
cigarette smoking
hypertension or anti HPT meds
low HDL
family history
age
ATP III Guidelines - Application
Step 4
If 2+ risk factors (other than LDL) without CHD or CHD equivalent,
assess 10-year CHD risk
Framingham tables
> 20% = CHD risk equivalent
ATP III Guidelines - Application
Step 5
Determine risk category
CHD or CHD Risk Equivalent
2+ Risk Factors
1-1 Risk Factors
Establish LDL goal
Determine need for TLC based on LDL
Determine level for drug consideration
ATP III Guidelines - Application
Step 6
Initiate TLC if LDL is above goal
TLC diet
Weight management
Increase physical activity
ATP III Guidelines - Application
Step 7
consider adding drug therapy if LDL exceeds recommended levels
Drugs + TLC simultaneously if CHD or CHD equivalent
Add drugs to TLC after 3 months for other risk categories
ATP III Guidelines - Application
Step 8
Identify metabolic syndrome and treat, if present after 3 months of
TLC
Clinical identification
abdominal obesity
hypertriglyceridemia
low HDL
hypertension
hyperglycemia
ATP III Guidelines - Application
Step 8 (cont.)
Treat underlying causes
weight management
physical activity
Treat risk factors if they persist despite TLC
treat hypertension
use asprin
treat hypertriglyceridemia, low HDL
ATP III Guidelines - Application
Step 9
Treat elevated triglycerides
primary aim is to reach LDL goals
intensify weight management
increase physical activity
consider TG lowering drugs
if TG > 500mg/dl, 1st lower TG to prevent pancreatitis (VLFD)
ATP III Guidelines - Application
Step 9 (cont.)
Treatment of low HDL
first reach LDL goal
intensify weight management and increase physical activity
consider drug treatment if TG normal
