Nutrition and
Cardiovascular Disease
Debbie S. Thompson MB.BS.
TMRU
Adapted by Dr L Chin-Harty
Cardiovascular Disease
Includes heart attack, stroke,
hypertension
 Leading cause of death in the U.S.
 Annually, 500,000 people die of
coronary heart disease in the U.S.
(1 million including strokes and
other CVD)

Atherosclerosis



Atherosclerosis is a progressive disease
involving the development of arterial wall
lesions.
As they grow, these lesions may narrow or
occlude the arterial lumen.
Complex lesions may also become unstable
and rupture, leading to acute coronary
events, such as unstable angina, myocardial
infarction, and stroke.
Pathophysiology of
Atherosclerosis




Plaque build-up can begin in childhood
Vessel lining is injured (often at
branch points) →
Plaque deposited to repair injured area
Plaque thickens, incorporating
cholesterol, protein, muscle cells, and
calcium (rate depends partly on level
of LDL-C in the blood) →
Pathophysiology of
Atherosclerosis



Arteries harden and narrow as plaque
builds, making them less elastic →
Increasing pressure causes further
damage →
A clot or spasm closes the opening,
causing a heart attack
Atherosclerosis Timeline
Foam
Cells
Complicated
Fatty Intermediate
Fibrous Lesion/
Streak
Lesion Atheroma Plaque
Rupture
Endothelial Dysfunction
From First
Decade
From Third
Decade
Adapted from Pepine CJ. Am J Cardiol. 1998;82(suppl 104).
From Fourth
Decade
Heart Attack
(Myocardial Infarction)



When blood supply to
the heart is disrupted,
the heart is damaged
May cause the heart to
beat irregularly or stop
altogether
25% of people do not
survive their first heart
attack
Symptoms of a Heart
Attack






Intense, prolonged chest pain or
pressure
Shortness of breath
Sweating, weakness
Nausea, vomiting and dizziness
(especially women)
Jaw, neck and shoulder pain
(especially women)
Irregular heartbeat
Factors that May Bring On a
Heart Attack in At-Risk Persons





Dehydration
Emotional stress
Strenuous physical activity when not
physically fit
Waking during the night or getting up
in the morning
Eating a large, high-fat meal
(increases risk of clotting)
Cerebrovascular Accident
(CVA)
Cerebrovascular Accident
Symptoms of Stroke





Sudden numbness or weakness of the face,
arm or leg, especially on one side of the
body
Sudden confusion, trouble speaking or
understanding
Sudden trouble seeing in one or both eyes
Sudden trouble walking, dizziness, loss of
balance or coordination
Sudden severe headache
Stroke Diagnosis
Hypertension:
Either:
 Systolic blood pressure ≥130 mmHg
(≥ 140 mmHg)
 Diastolic blood pressure ≥ 80 mmHg (≥
90 mmHg)
– ACC/AHA 2017
Blood Lipid Levels are
Related to Risk of CVD
Lipoproteins
Lipids cannot mix with water and blood is high in
water
 As lipids cannot travel in blood without help,
lipoproteins are formed to carry lipids
Consist of:
1.
Lipids (triglycerides, cholesterol)
2.
Protein
3.
Phospholipids

Lipoprotein Summary
Low-Density Lipoproteins
(LDL-C)





Also called “bad cholesterol”
Contain relatively large amounts of fat,
and less protein
Deposits cholesterol in arteries
Thus, ↑ LDL-C is associated with ↑
CVD risk
Serum LDL-C should be <3.4 mmol/L
High-Density Lipoproteins
(HDL)





Also called “good cholesterol”
Relatively high in protein, lower in lipid
Acts as scavenger, carrying cholesterol from
arteries to liver
– Liver packages as bile
– Excretes
↑ HDL-C is associated with ↓ risk of CVD
Optimal serum HDL-C should be approx 1.5
mmol/L
Triglycerides



The most diet-responsive blood lipid
Should be ≤150 mg/dL (1.69 mmol/L) in
fasting state
Conversion factor =88.6
Total Cholesterol



Includes HDL-C, LDL-C, and a fraction
of the triglycerides
Total cholesterol should be ≤ 200
mg/dL (5.2 mmol/L) when fasted
Total cholesterol does not tell whole
story
Total Cholesterol


John and Marty
each have total
cholesterol levels of
200 mg/dL.
Their health risk is
different
Total Cholesterol is Not
Enough
John’s Lipid Profile
 TC: 200 mg/dL
 LDL-C: 140 mg/dL
 HDL-C: 30 mg/dL
 TG: 150 mg/dL
Marty’s Lipid Profile
 TC: 200 mg/dl
 LDL-C: 95 mg/dL
 HDL-C: 75 mg/dL
 TG: 150 mg/dL
What Affects Cholesterol
Levels?





Diet
Weight
Physical activity
Age and gender
Heredity
You control the first three!
Evaluating Blood Lipids
Risk Factors for CVD









Cigarette smoking
Hypertension or anti-hypertensive rx
High LDL levels
Low HDL-C
Family history of premature coronary heart disease in
first degree relative (in male <55 years, in female <65
years)
Age (men ≥45 years, women ≥55 years)
Diabetes (considered equivalent to a history of CHD)
Obesity
Inactivity
Source: ATP-III Guidelines, NHLBI, accessed 2-2005
Screening for CVD Risk




Everyone 20 and older should have his
cholesterol measured at least every 5
years
Lipoprotein profile: includes TC, LDL-C
HDL-C and TG
At least should include TC and HDL-C
If TC> 200 mg/dL or HDL-C< 40
mg/dL, obtain full lipid profile
Source: National Cholesterol Education Program, National Institutes of
Health, accessed 2-05
Harmful dietary fat
Saturated fatty acids (SFAs)



Most saturated fats are solid at room
temperature
Found in animal products (dairy, poultry
with skin, butter, lamb and beef fat) and
contain cholesterol.
Unlike animal fats, palm and coconut oils
are saturated fats that are called oils but
depending on room temperature can be
solid, semi-solid, or liquid, and do not
contain cholesterol.
Harmful dietary fat
Saturated fatty acids (SFAs)



Raise total blood cholesterol levels and
LDL cholesterol levels
May also increase the risk of type 2
diabetes.
SFAs are also associated with CAD
progression
Coconut Oil



Coconut oil contains 91% SFAs and only 6%
MUFAs and 2% PUFAs.
Unlike virgin coconut oil, refined coconut oil
(used for home cooking, commercial food
processing, and cosmetics) has no coconut
taste or aroma.
Refined Bleached Deodorised coconut oil can
be partially hydrogenated to increase its
melting point. During this process, some of
the MUFAs and PUFAs are transformed into
trans fatty acids.
Coconut Oil
2. Harmful dietary fat:
Trans fats






50% of trans-fatty acids come from animal foods
(beef, butter, milk fats)
Trans fats are made during food processing through
partial hydrogenation of unsaturated fats.
This process creates fats that are easier to cook with
and less likely to spoil than naturally occurring oils.
Synthetic trans fat can increase LDL cholesterol and
lower HDL cholesterol.
Major foods sources in US are stick margarine,
shortening, commercial frying fats, high fat baked
goods
Has less of a cholesterol raising effect than SFA
Healthier dietary fats
Monounsaturated fatty acids
(MUFAs)
Found
in a variety of foods and oils; canola oil,
avocado, olives, pecans, peanuts, and other nuts
 Oleic acid is the most prevalent MUFA in the US
diet
Improve blood cholesterol levels, may benefit
insulin levels and blood sugar control
 Mediterranean diet: high in fat, especially
MUFA (olive oil), fish, nuts, low in red meat
associated with ↓ risk of CVD
Healthier dietary fat
Polyunsaturated fatty acids
(PUFAs)
Found
mostly in plant-based foods and
oils
Improve blood cholesterol levels
Help decrease the risk of T2D.
May also protect against irregular
heartbeats and help lower blood pressure
levels.
Omega-3 PUFAs ( EPA, DHA)


One type of PUFA, (omega-3 fatty acids) appears
to decrease the risk of coronary artery disease.
Sources
– Fatty fish (salmon, tuna), fish oil supplements
– Canola and soybean oil**
– Flaxseed, walnuts
Examples:
eicosapentaenoic acid (EPA) and
docosahexaenoic acid (DHA)
Omega-3 Fatty Acids






One fatty fish meal/week resulted in
50% decrease in risk of cardiac arrest
1 g supplement of omega-3 daily
reduced risk of CVD, nonfatal MI,
nonfatal stroke
Anticoagulant effect
Decrease vasoconstriction
Improve endothelial dysfunction
Reduce inflammation
Prevention and Management of
Hypertension






Maintain a healthy weight.
Be physically active.
Follow a healthy eating plan.
Drink alcohol only in moderation.
Take prescribed drugs as directed.
Eat foods with less sodium (salt).
NHLBI Patient Guidelines, accessed 2-05
Low salt
The Dietary Guidelines for Americans
recommend limiting sodium to less than
2,300 mg a day - or 1,500 mg if
you're:
 age 51 or older
 black
 have high blood pressure
 diabetes or chronic kidney disease.
Sources of salt



Processed foods: typically high in salt and
additives that contain sodium (bread, prepared
dinners like pasta, meat and egg dishes, pizza,
cold cuts and bacon, cheese, soups, and fast
foods)
Natural sources: All vegetables and dairy
products, meat, and shellfish (1 cup of low-fat
milk has about 100 mg of sodium)
Condiments: One tablespoon (15 ml) of soy
sauce, for example, has about 1,000 mg of
sodium.
DASH: Dietary Approaches
to Stop Hypertension





Eat foods that are low in fat, saturated
fat and cholesterol
Eat more fruits, vegetables, whole
grains, and low fat dairy products
Eat more poultry, fish, nuts, and
legumes
Eat less red meat, fats, sweets, and
sugared beverages
Eat foods low in sodium
NHLBI. DASH Eating Plan, revised 2003. Accessed 2-2005
Lowering LDLs




Visit doctor to assess for other
conditions
Reduce dietary saturated fat, trans
fatty acids, and cholesterol
Increase MUFA and PUFA
Increase dietary fiber
Raise the HDL






Physical activity
At least 45 min./day, 4 days a week
Avoid smoking
Eat regularly
Eat less total fat
Moderate intake of alcohol increases
HDL
Lowering Blood TG








TG is the most diet-responsive blood lipid
Avoid overeating
Limit alcohol and simple sugars
Small frequent meals
Include fatty fish in the diet
Control diabetes if present
Perform regular physical activity (30 minutes
on most, if not all, days)
No smoking
Other Recommendations






Fat intake can be higher as long as saturated
and trans fatty acids are minimal
Reduce simple sugars and refined CHO
Choose chicken breast or drumstick instead of
wing and thigh
Select skimmed milk (1%) instead of whole
milk (2%)
Buy lean cuts of meat such as round, sirloin,
and loin
Read nutrition labels on food packages
Healthy Cooking





Bake, steam, roast, broil, stew or boil
instead of frying
Remove poultry skin before eating
Use a nonstick pan with cooking oil spray
or small amount of liquid vegetable oil
instead of lard, butter, shortening, other
solid fats
Trim visible fat before you cook meats
Chill meat and poultry broth until fat
becomes solid, remove
Dining Out





Choose restaurants with low-fat options
Ask that sauces, gravies, and salad dressings
be served on the side
Control portions sizes
At fast food restaurants, choose salads,
grilled (not fried or breaded) skinless chicken
sandwiches, regular-sized hamburgers, or
roast beef sandwiches
Avoid regular salad dressings and fatty
sauces.
Other Dietary Interventions

Cholestin® differs from the traditional red rice yeast that
is sold in Chinese groceries which contains much lower
amounts of statins. It is manufactured by growing a
single strain of M. purpureus on rice under carefully
controlled conditions that increase the statin content.

Plant Stanols/Sterol Esters
 Decrease absorption of cholesterol and lowers amount
returning via enterohepatic circulation.
 Benecol® and Take Control® margarine
Drug Treatment


Statins: (e.g. Lovastatin, Pravastatin) a class
of drugs used to lower cholesterol levels by
inhibiting HMG-CoA reductase, which plays a
central role in the production of cholesterol in
the liver.
Bile acid sequestrants: (eg. cholestyramine)resins used to bind components of bile in the
GIT. They disrupt the enterohepatic
circulation of bile acids by combining with bile
constituents and preventing reabsorption from
the gut.
Drug Treatment


Nicotinic acid/niacin: Nicotinic acid
reduces the production of triglycerides
and VLDL. Nicotinic acid raises HDL-C
more than other lipid-lowering
medicines.
Fibric acids: are used as adjunct in
hypercholesterolemia, usually in
combination with statins. Used mainly
to lower triglycerides and raise HDL-C
(Gemfibrozil or fenofibrate)
Phytochemicals

Chemical compounds that occur naturally in plants.
Some are responsible for color, odour and other
properties.

They have biological significance (eg. antioxidants) not established as essential nutrients.

There may be as many as 10,000 different
phytochemicals having the potential to affect
diseases such as cancer, stroke or metabolic
syndrome.
Phytochemicals



↓ inflammation
↓ blood clotting
Include anthocyanins (found in red and blue
fruits such as raspberries and blueberries
and vegetables) lutein (green leafy
vegetables) lycopene (tomato products),
phenolics (citrus fruits, fruit juices, cereals,
legumes, and oilseeds)
Mediterranean Diet and
CVD






High in fruits, vegetables, whole
grains, beans, nuts, seeds
Olive oil as a source of
monounsaturated fats
Low to moderate wine consumption
Low to moderate fish, poultry, dairy
products
Little red meat
Use of herbs and spices with less salt
Nutrition in the
Sickle Cell Unit
Jamaica
Critically ILL Patients
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
1
Starvation
Tropical Medicine Research Institute
The University of the West Indies
Sickle Cell Unit
Jamaica
Dr. Marvin Reid MB BS PhD
2
65 kg Man
Body
Content
Sickle Cell Unit
Jamaica
Store
Kcal
600
CHO
500g
Prot
11000g 9600
Fat
9000g
Exhaustion
Time (d)
All in 24hr <1
Daily
utilization
60
58500 150
Assumes energy expenditure of 1600 kcal/d
Tropical Medicine Research Institute
The University of the West Indies
~40
~40
Cori cycle
Tropical Medicine Research Institute
The University of the West Indies
Sickle Cell Unit
Jamaica
Glucose Production
Tropical Medicine Research Institute
The University of the West Indies
Sickle Cell Unit
Jamaica
Starvation fat Metabolism
Sickle Cell Unit
Jamaica
Acetyl CoA
Oxalacetate
Citrate
Kreb cycle
Tropical Medicine Research Institute
The University of the West Indies
Acetoacetate
β-Hydroxybutyrate
Fatty Acids
Liver PTO
„
Protein free diet but adequate energy
„
„
„
„
„
„
Sickle Cell Unit
Jamaica
Liver loses protein immediately
No change in fsr
Next 3 weeks – rate of loss decreases + increase in fsr
Starvation – protein synthesis falls by 30% in two
days
Alteration in diurnal variation
A small decrease in albumin conc ~6 Month
Tropical Medicine Research Institute
The University of the West Indies
Decrease in PTO
„
„
„
Sickle Cell Unit
Jamaica
Energy savings ~70 kcal assuming 15% of
BMR goes to PTO
Decrease demand for dietary AA
Lesser loss of AA through oxidation
Tropical Medicine Research Institute
The University of the West Indies
Effect of starvation
„
Sickle Cell Unit
Jamaica
Decrease resistance to infection
„
„
„
„
Increase translocation in GIT
Disproportionate depletion of lymphoid tissue
Decreased ability to synthesize immunoglobulin
Increased oxidative stress
Tropical Medicine Research Institute
The University of the West Indies
Injury
Sickle Cell Unit
Jamaica
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
10
Response to injury
„
„
„
Sickle Cell Unit
Jamaica
Characteristic metabolic response to injury
whether 2˚ to trauma burns, infection or
sterile inflammatory processes
Associated with hypermetabolism & wasting
If prolonged
„
„
„
Immunosuppression
Delayed wound healing
Death
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Nutrition support in the early
stages may mitigate these
potential adverse effects
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
12
Starvation vs Critical illness
Sickle Cell Unit
Jamaica
Starvation
Critical illness
BEE
↓
Glucose utilization
limited
Normal or ↓
initially then ↑
↑
Fatty acid utilization ↑
↑
Ketone Utilization
↑
↓
Gluconeogenesis
Muscle protein
catabolism
↑ initially, ↑
↓ After 5-7
days
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Ebb
„
Sickle Cell Unit
Jamaica
Begins at injury
„
„
„
„
„
↓ volume
↓ metabolic rate
↓ core temperature
↓ cardiac output
last 24-48 hrs
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Flow phase
„
Sickle Cell Unit
Jamaica
Begins after ebb
„
„
„
„
„
„
↑ metabolic rate
↑ core temperature
↑ cardiac output
↑ conc of cortisol,epinepherine
↑ conc of cytokines & other inflammatory
mediators
Duration a function of insult but peak 3-4 dys,
duration 7-10 dys
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Increase in BEE
Tropical Medicine Research Institute
The University of the West Indies
Sickle Cell Unit
Jamaica
Dr. Marvin Reid MB BS PhD
Protein
„
„
„
Sickle Cell Unit
Jamaica
↑ protein synthesis & ↑↑ protein
catabolism=net loss =~20 gN/d
Repriorization of visceral protein synthesis
Glutamine & alanine ~70% of AA released
from skm
„
„
„
Glut=fuel for gut & immune cells
ALA =hepatic gluconeogenesis
BCAA=oxidative fuel
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Protein Loss
Tropical Medicine Research Institute
The University of the West Indies
Sickle Cell Unit
Jamaica
Dr. Marvin Reid MB BS PhD
Glucose & trace elements
„
„
„
Sickle Cell Unit
Jamaica
↑ gluconeogenesis & lipolysis
hyperglycaemia – hepatic glycogenolysis, ↑
gluconeogenesis & insulin resistance
Alteration in trace element metabolism
„
↓plasma conc of Fe, Zn, PO4, Mg2+,
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Aim of nutritional support
„
„
Sickle Cell Unit
Jamaica
Alteration in nutritional status may occur
because of inadequate intake eg starvation or
alteration in metabolism of substrates
Aim
„
Prevent malnutrition from becoming a major
cofactor in organ dysfunction and in mortality &
morbidity
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Nutritional Paradigm
Sickle Cell Unit
Jamaica
Mismatch between Intake and Demand
Alteration in form and Function
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Alteration in Form
„
„
„
Sickle Cell Unit
Jamaica
Loss of LBM
Loss of fat mass
Organ changes
„
„
Muscle - loss of type 2 fibres
GIT-Loss of mucosal architecture - ↓ villus
height, ↓ Crypt depth & impaired barrier function
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Alteration in Function
„
Sickle Cell Unit
Jamaica
Alteration in function often precedes
measurable change in composition
„
„
„
„
Immune function- T cell, APP response
GIT - Barrier function
Resp function –VO2 max, maximal insp & exp
pressures
Cardiac - bradycardia, low CVP, low BP
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Physical Examination
„
„
„
„
Signs of wasting
Signs of specific nutrient deficiency
Signs of major system dysfunction
Assessment of muscle strengh
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Energy Needs
„
Measure
„
„
„
Sickle Cell Unit
Jamaica
Indirect Calorimeter
Estimated using regression equations
Protein
„
„
Measure with 24 hr urine
Estimate
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Management
„
„
Sickle Cell Unit
Jamaica
Ebb phase – cardiopulmonary resusication
Flow – aim to reduce hypermetabolim and
catabolism of flow phase
„
„
Early nutrition within 24-48 hrs preferable by
enteral route
Enteral formulas vary in caloric density, fiber
content, source of protein and fat,
immunonutriticals, osmolality
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Nutritional support
„
„
Supplemental feeding
Forced feeding
„
„
Enteral
Parenteral
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Enteral
„
Feed Type
„
„
„
„
Sickle Cell Unit
Jamaica
NGT or NJ
Gastrostomy /PEG
Jejunostomy
Choice of feed
„
„
„
„
Osmolarity
Caloric density
Fibre
Special formulas
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Early nutrition
„
Sickle Cell Unit
Jamaica
Early nutrition feeding within 24 hrs
„
„
↓incidence of infections
↓length of hospital stay
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
TPN better than late EN
Sickle Cell Unit
Jamaica
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Immunonutrition
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
32
Sickle Cell Unit
Jamaica
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Lipid
Unsaturated fats
Saturated fats
No double bond
Sickle Cell Unit
Jamaica
No double bond
Monosaturated (MUFA) eg
Oleic acid
LCA –mainly
from animal
PUFA
MCT –coconut oil;
easily digested &
absorped
N-3 or omega 3 eg linoleic
SCFA-produced
by colonic flora
N-6 or omega 6 eg linoleic
Vegetable source eg corn, soy
Fish oils – N-3 PUFA
Eicopentaenoic acid (EPA)
Tropical Medicine Research Institute
The University of the West Indies
TROPICAL MEDICINE
Docosahexaenoic
RESEARCH INSTITUTE
acid (DHA
Effects of Lipids
Sickle Cell Unit
Jamaica
Intensity of inflammatory effect
•
N-6 PUFA
Pro inflammatory
•
•
MUFA
N-3 PUFA
Anti inflammatory
Eicosapentaenoic
Acid(EPA)
It is an Omega 3 fatty
acid(metabolite of alphalinolenic acid)
Reduce the levels of
arachidonic acid in cells
reducing the production of
proinflammatory
eicosanoids
Sardine oil
Tropical Medicine Research Institute
The University of the West Indies
•
TROPICAL MEDICINE
RESEARCH INSTITUTE
Effect of Immunonutrition on Mortality in
22 Trials
Sickle Cell Unit
Jamaica
P value for homogeneity is .54
Tropical Medicine Research Institute
The University of the West Indies
TROPICAL MEDICINE
RESEARCH INSTITUTE
Heyland et al JAMA 2001
Effect of Immunonutrition on infectious
complications in 22 Trials
Sickle Cell Unit
Jamaica
P value for homogeneity is <0.001
Tropical Medicine Research Institute
The University of the West Indies
TROPICAL MEDICINE
RESEARCH INSTITUTE
Heyland et al JAMA 2001
Conclusion
„
„
„
Sickle Cell Unit
Jamaica
Nutrition plays important role in recovery of
critically ill patients
Enteral nutrition is the preferred route
The practice is evolving & becoming more
sophisticated
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Nutrition & GI
Sickle Cell Unit
Jamaica
Clinical Nutrition
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
1
Objectives


Sickle Cell Unit
Jamaica
Review of GI
Physiology
Nutritional
management of
selected GI diseases
eg




Dumping syndrome/
pancreatitis /
Short Bowel Syndrome/
Liver disease
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Amplification of the surface area of the
human small intestine
Cylinder
x1
3,300 cm2
Folds
x3
10,000
cm2
Villi
x10
100,000
Microvilli
x20
2,000,000
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Intestinal cell renewal



Sickle Cell Unit
Jamaica
Dividing mucosal cells are found near the crypt
region
Following proliferation, cells migrate to the base of
the crypt to become paneth cells or the villous
region where they become progressively
differentiated and assume various digestive and
absorptive function
Turnover =48-72hrs
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Function of Intestinal epithelium






Barrier and immune function
Fluid & electrolyte absorption
Protein synthesis
Nutrient digestion & absorption
Fluid & electrolyte secretion
Mediator production
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Fluid Flux in GIT
Sickle Cell Unit
Jamaica
Intake
~2L
Gut Secretions
~7L
Total
~9L
Absorption
Small intestine
~7.5L
Colon
~1.3L
Output
~0.2L
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Water movement



Sickle Cell Unit
Jamaica
The intestinal mucosa acts as a
semipermeable membrane (size of tight
junction)
Water movement is passive and follows solute
movement
Mucosal permeability varies along length of
intestine highest in jejenum & lowest in colon
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sodium Absorption

Na-H Exchange


Na-dependent Co-transport


Small bowel /post prandial
Coupled Na-C / Absorption


Proximal small bowel/Non-nutrient
Ileum,colon
Na Channel

Distal colon
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Sodium dependent cotransport


Na-glucose cotransporter in the luminal
membrane
Basis of ORF
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
NA Flux in GIT
Sickle Cell Unit
Jamaica
Intake
~150 mmol
Gut Secretions
~1000 mmol
Total
~1150 mmol
Absorption
Small intestine
~950 mmol
Colon
~195 mmol
Output
~5 mmol
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Potassium



Sickle Cell Unit
Jamaica
Overall K+ movement is the result of solvent
drag and is potential-dependent
Active K+ secretion occurs in the colon
Recto-sigmoid has an active K+ absorptive
process most likely K-H exchange
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Chloride

Potential-dependent Cl absorption



Sickle Cell Unit
Jamaica
Jejenum & ileum
Coupled Na and Cl absorption
HCO3 dependent Cl absorption

Ileum / colon / rectum
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
K & Cl Fluxes in GIT
K
CL
Intake
80 mmol
150
Gut
Secretions
Total
40 mmol
750
120 mmol
900
110 mmol
800
-3 mmol
97
13 mmol
3
Absorption
Small
intestine
Colon
Output
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Major areas of nutrient
absorption

Carbohydrate


Lipid/Protein


Duodenum/jejenum
Iron


Duodenum/jejenum
Duodenum
Bile salts

Ileum
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Carbohydrate absorption
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Glu transporters


Sickle Cell Unit
Jamaica
SGLT1 (Sodium-dependent glucose cotransporter) upregulated by luminal Glucose. Related to glucose
transporter in renal tubule
GLUT2 (glucose transporter)– facilitated diffusion
exit at basolateral membrane
Basolateral
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Regulated translocation of GLUT2 in food-facing enterocyte membranes.
Sickle Cell Unit
Jamaica
Leturque A et al. Am J Physiol Endocrinol Metab
2009;296:E985-E992
©2009 by American Physiological Society
Tropical Medicine Research Institute
The University of the West Indies
Fat luminal digestion &
absorption





Sickle Cell Unit
Jamaica
Emulsification by bile salts
Lipolysis –lipase
Micelle formation
Release of fatty acid & monoglycerides from
micelle and diffusion into mucosal cell.
Mucosal uptake- Binding to fatty acid binding
protein aids
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Intramucosal aspect of fat
absorption



Sickle Cell Unit
Jamaica
Re-esterification –cytoplasmic carrier proteins
to Smooth endoplasmic reticulum (sER)
Chylomicron & VLDL formation
Secretion- into intestinal lacteals
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Medium Chain Triglycerides




Sickle Cell Unit
Jamaica
8-10 carbons
Micellar formation not required
No reesterification in mucosal cell
Transported in the portal blood as free fatty
acid
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Protein digestion & absorption



Sickle Cell Unit
Jamaica
Pancreatic proteolytic enzymes break
proteins into oligopeptides and AA
Brush border peptidases hydrolyze
oligopeptides into di and tri peptides
Di and tripeptides are absorbed across
mucosal cells
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Peptide & AA absorption
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Defects asociated with
Malabsorption




Impairment of mechanical digestion
Impairment of chemical digestion
Impairment of solubilization
Anatomic/Pathologic impairment of
absorption
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Conclusion

Sickle Cell Unit
Jamaica
The GIT is very active metabolic organ that is
adapted for its role in digestion & absorption
of nutrients.
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Dumping Syndrome


Sickle Cell Unit
Jamaica
Pyloric sphincter bypass
Symptoms –


Early during a meal or within 30 minutes
Late ~ 3hrs after a meal









Nausea
Vomiting
Abdominal pain, cramps
Diarrhea
Dizziness, lightheadedness
Bloating, belching
Fatigue
Heart palpitations, rapid heart rate
Hypoglycaemia & mental confusion may occur as late symptoms
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
enteroglucagon, peptide YY, pancreatic
polypeptide, vasoactive intestinal polypeptide,
glucagonlike peptide-1 (GLP-1), neurotensin,
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Nutrition Therapy



Sickle Cell Unit
Jamaica
Limit simple sugars
Emphasize high protein high fat foods
Eat small frequent meals
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Pancreatitis


Sickle Cell Unit
Jamaica
Mild pancreatitis - Usually self-limiting ;
Nutrition appears not to affect clinical
outcome; Enteral nutrition tolerated and may
be associated with less adverse effects.
Severe pancreatitis - TPN is preferred
especially if fistula develops. Lipid safe
provided baseline TG results normal
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Severe Pancreatitis




Sickle Cell Unit
Jamaica
Chronic Pancreatitis
20 -30% develop DM
pancreatic exocrine insufficiency lipase(<10%) + tyrpsin
Low fat diet, MCT, pancreatic enzymes, H2Blockers,antibiotics if Small Bowel Overgrowth
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Short Bowel Syndrome

Sickle Cell Unit
Jamaica
Clinical syndrome produced by loss of
mucosal absorptive area and shortened
intestinal transit time due to resection.

diarrhoea, wt loss, malnutrition, steatorrhea.
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Short Bowel Syndrome

The effect is dependent upon





site of resected bowel
whether both ileum and colon resected
extent of resection
functional capabilities of remaining bowel
adaptation of remaining bowel
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Short Bowel Syndrome


Sickle Cell Unit
Jamaica
Patients with jejunostomy and <100 cm of
jejunum usually require permanent TPN
Patients with intact colon and <50 cm of
jejunum usually require permanent TPN
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
SBS-Management Principles




Sickle Cell Unit
Jamaica
<30% resection with colon-usually no significant
nutritional effect;low oxolate diet;vit B12
30-50% resection with colon- fat restricted, low
oxolate; enteral therapy
>50% resection with colectomy - TPN initially;
enteral intake 50-100% expected goals. elemental
diet vs polymeric diets
>75% -TPN
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Malnutrition in cirrhosis
Sickle Cell Unit
Jamaica
Decrease in oral intake:
 Anorexia, nausea, vomiting, early satiety, taste
abnormalities,alcohol abuse, iatrogenic due to restrictive
diets or NPO status, medications
 Maldigestion and malabsorption:
 Fat malabsorption due to cholestasis or chronic
pancreatitis.
 Water-soluble vitamin malabsorption due to alcohol
abuse.
 Calcium- and lipid-soluble vitamin malabsorption due to
cholestasis.
 Metabolic abnormalities:
 Glucose intolerance, increased protein and lipid
catabolism
similar
to sepsis, trauma or other catabolic
Tropical Medicine
Research
Institute
Dr. Marvin Reid MB BS PhD
states.
The University
of the West Indies

Liver Disease
Sickle Cell Unit
Jamaica
Protein
Energy goal
Hepatitis
1-1.5
30
Prevent malnutrition
Cirrhosis
1-1.5
30
Prevent malnutrition
Treat fat malabsorption
30
Provide nutritional needs
without encephalopathy
Encephalopathy 0.5-0.75
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Principles of Nutrition Support
Prof. Marvin Reid MB BS PHD
Prof. Marvin Reid MB BS PhD
Objectives
• Define malnutrition
• Identifying individuals at nutrition risk
• Principles of Nutrition assessment
• Administering Nutrition support
Prof. Marvin Reid MB BS PhD
Malnutrition-definition
• Mismatch between intake and demand leads to
alteration in form and function
• Malnutrition - A state of nutrition in which a
deficiency, excess or imbalance of energy, protein
or other nutrients including minerals and vitamins
causes measurable adverse effects on body
function and clinical outcome.
Prof. Marvin Reid MB BS PhD
Malnutrition
• Malnutrition
• Severe undernutrition ~1% in JA
• ~40% in hospitalized patients
• Overnutrition-21% in JA
• Consequence
•
•
•
•
Increased mortality & morbidity
decreased immune competence & poor wound healing
Psychological & cognitive effects
Increased Health Care Cost
Prof. Marvin Reid MB BS PhD
Objectives
• Define malnutrition
• Identifying individuals at nutrition risk
• Principles of Nutrition assessment
• Administering Nutrition support
Prof. Marvin Reid MB BS PhD
Clinical nutrition Mx pathway
Screening
Assessment
Treatment
Monitoring and Evaluation
Prof. Marvin Reid MB BS PhD
Screening algorithm-ASPEN2002
Prof. Marvin Reid MB BS PhD
Aim of Screening
• Identifying patients at increased risk for
malnutrition
• Risk of malnutrition
• Stress or hypermetabolism without adequate food
intake
• Weight loss >10% of usual body weight
• BMI <22 kg/m2
• Low albumin <35 g/l
• Prolonged NPO >7 days
• Absence of – (i)Ability to swallow,(ii) functional GUT,
(iii)poor oral intake.
Prof. Marvin Reid MB BS PhD
Nutrition screening tools
• SGA –Subjective Global Assessment
• Validated in GI Surgery Patient
• Used for screening & assessment
• MUST –Malnutrition Universal Screening Tool
• Validated for Hospitalized and Community care setting
• NRS 2002-Nutrition Risk Screening
http://www.bapen.org.uk/must_tool.html
• Validated in Hospitalized Patients
Prof. Marvin Reid MB BS PhD
Prof. Marvin Reid MB BS PhD
Prof. Marvin Reid MB BS PhD
NRS 2002
Clinical Nutrition 2003;321-336
Prof. Marvin Reid MB BS PhD
Objectives
• Define malnutrition
• Identifying individuals at nutrition risk
• Principles of Nutrition assessment
• Administering Nutrition support
Prof. Marvin Reid MB BS PhD
Nutritional assessment measure
• Ideally nutrition assessment parameter should be
unaffected by factors unrelated to nutrition, and
correlates with response to nutrition therapy
• No single assessment measures sufficiently
sensitive or specific for malnutrition
• Combination of subjective & objective measures
Prof. Marvin Reid MB BS PhD
Anthropometry
• Weight
•
•
•
•
Body weight
Ideal body weight
Adjusted body weight (obese)
BMI
• Skinfolds & Circumferences
• BIA
Prof. Marvin Reid MB BS PhD
Bioelectric impedance
Prof. Marvin Reid MB BS PhD
Physical Examination
• Inspection
• Palpation
• Percussion
• Ascultation
Prof. Marvin Reid MB BS PhD
Biochemistry
• Serum proteins
• Albumin,transferrin,throxine-binding
globulin,prealbumin,retinol binding protein
• Hepatic derived liver protein
• Affected by non-nutritional factors such as hydration,
infection, bleeding fever, hormones
• Creatinine-height index
• N2 balance
Prof. Marvin Reid MB BS PhD
Albumin
• Visceral proteins do not define
malnutrition
g/l
45
40
35
30
25
20
15
10
5
0
1
2
3
Experiment
Albumin FSR
25
20
%d
• In anorexia nervosa albumin conc
unchanged
• Gil et al : Nutrition 1997-Albumin
reflect changes in ECW
• Clark et al JPEN 1996- Does not
respond to refeeding
• Morlese et al AJCN1996-Albumin
concentrations but not FSRs were
lower in studies 1 and 2 than in
study 3
Albumin Concentration
15
10
5
0
1
2
Experiment
3
Risks of Albumin Therapy
Cochrane Injuries Group Albumin Reviewers BMJ 2011
Prof. Marvin Reid MB BS PhD
Surgical site & malnutrition
pancreas
oesophagus
Gastric
colon
Kudsk et al JPEN 2003
Prof. Marvin Reid MB BS PhD
Objectives
• Define malnutrition
• Identifying individuals at nutrition risk
• Principles of Nutrition assessment
• Administering Nutrition support
Prof. Marvin Reid MB BS PhD
Nutrition support
Prof. Marvin Reid MB BS PhD
Veteran Coop study 1991
Preop feeding 7-15 days
%
Main outcomes
45
40
35
30
25
20
15
10
5
0
N Eng Med vol 325 1991
TPN; n=192
Control; n=203
Major
Infectious
Complications Complication
Infectious
Complication
in severe malnutrition
Prof. Marvin Reid MB BS PhD
Maastricht trial
preop feeding~12 days
• Malnourished patients in the intervention arms
only
• 4 groups TPN preop (n=51), TEN preop (n=50), No
nutrition (n=50) and a control non-nutritional
depleted group (n=49)
• No differences in complication rates between the
groups.
• More Septic complications in TPN >TEN if weight
loss >10%
Clin nutr ,1992
Prof. Marvin Reid MB BS PhD
Goal of nutrition support
• Improve Clinical Outcome
• To prevent starvation-induced complications
• To favourably alter the natural history or treatment of a
specific disease process
Prof. Marvin Reid MB BS PhD
Specific aims of nutrition support
•  rate of weight loss and protein breakdown
(catabolic patients)
• Maintain body wt and protein stores –pt who
cannot eat for prolonged periods
• Weight gain & anabolism –prem infant, depleted
patients
Prof. Marvin Reid MB BS PhD
Methods of Nutrition Support
• Enteral
• Parenteral
Prof. Marvin Reid MB BS PhD
Body Composition Changes in response to
10 days TPN
Body Composition Changes
Mean Difference kg
5
Weight
Water
Protein
Fat
0
-5
-10
-15
Intake 2750 kcal & 127 g protein
Streat et al J trauma 1987
Prof. Marvin Reid MB BS PhD
Nitrogen Supply
Mean Nitrogen balance on Days 2-8
Nitrogen intake (g /kg body weight/d)
Nitrogen Balance (gN)
0
0.1
0.2
0.25
*
*
0.3
0
-5
-10
*
*
Larsson et al Br. J Surg 1990
-15
Prof. Marvin Reid MB BS PhD
When
Prof. Marvin Reid MB BS PhD
Early Postoperative feeding
• Moss 1981 JPEN
• Colectomy
• Post op feeding 5±3 hrs
into duodenum
• oral feeding 17-24 hrs
• Active management of
ileus
Early enteral feeding versus “nil by mouth” after gastrointestinal surgery: systematic review and
meta-analysis of controlled trials
BMJ. 2001 October 6± 323 (7316): 773
Stephen J Lewis et al
vomiting
Anastomotic dehiscence
Hospital Stay
difference
Infection
0.0
0.5
N=837 patients & 11 studies
1.0
Odds Ratio
Prof. Marvin Reid MB BS PhD
1.5
How
Prof. Marvin Reid MB BS PhD
Sir Christopher Wren 1656
• “The most considerable experiment
I have made of late… I injected wine
and ale into the mass of blood of a
living dog, by vein in good
quantities, till I made it extremely
drunk, but soon he pissed it out”
Parenteral Nutrition Substrates
• CHO Source
• Dextrose -20-70% (3.4 kcal/g)
• Glycerol
• Protein Source
• Crystalline AA
• Standard – balance mixture of essential & non-essential. 315%.
• Modified – designed to meet disease or age-specific AA
requirements
• Dipeptides- More soluble than AA
Prof. Marvin Reid MB BS PhD
Fat source
• Fat
• Long chain fatty acid emulsions made from either
soybean oil or a mixture of safflower and soybean oils.
10%, 20% and 30%.
• MCFA / LCFA mixtures- fat source containing MCFA + fat
source containing LCFA
• MCFA-LCFA structured lipid
Prof. Marvin Reid MB BS PhD
Electrolytes
• Electrolytes
• Na= 0-150 mmol/l
• K=0-100 mmol/l
• Ca =0-7.5 mmol/l
• Mg =0-7.5 mmol/l
• Po4=0-10 mmol
Factors affecting conc
Patient clinical condition, compatibility
Prof. Marvin Reid MB BS PhD
Vitamin & Trace Element
• Vitamin
• Multidose
• Single dose
• Trace element
• Multidose
• Single dose
Prof. Marvin Reid MB BS PhD
Parenteral Nutrition Formulations
• 2-in-1 = dextrose + AA +
additives
• Lipids if given is piggy backed.
• Lipid max infuse time when
given this way=12hrs.
• Give using a blood giving set
22 ul filter
Prof. Marvin Reid MB BS PhD
TPN 3 in 1 Admixture
• 3-in-1 (TNA)=Total nutrient admixture
• Lipid+ dextrose + AA + additives in one container
• Advantages
•  Nursing time, risk of contamination, catheter infection, cost
• Better lipid utilization
• Disadvantages
• Stability
• Compatibility
• Filtration – 1.2 µm rather than 0.22µm
Prof. Marvin Reid MB BS PhD
Stability
• Temperature
• pH
• Light
• Composition
Prof. Marvin Reid MB BS PhD
Types of PN
• Central Parenteral Nutrition
• Delivers nutrient into central vein
• High osmolarity allowed
• Peripheral Parenteral Nutrition
• Delivers nutrient into peripheral vein
• Typically for duration < 1 week
• Max osmolarity <900 mOsmol/l
Prof. Marvin Reid MB BS PhD
TPN indications
• Absolute
• GI failure
• Relative
• fistula, crohns disease,
severe pancreatitis
TPN
• Indication - GI failure
• Usually mixed to precise specification
•
•
•
•
100 g glu/dy rate should be <5-7 mg/kg/min
Lipid ~ < 30% of total calories
NPC to N ~100:1
TEN approach for calculations
• Type
• CPN
• PPN
Prof. Marvin Reid MB BS PhD
TPN 2
• Benefits
• Best if duration of support >=5-7 days
• Home TPN
• Complications
• More infectious complications cf enteral
• Catheter related
• Metabolic –glucose, lipid, AA, fluid
Prof. Marvin Reid MB BS PhD
Enteral Nutrition
Prof. Marvin Reid MB BS PhD
Enteral Nutrition Routes
Prof. Marvin Reid MB BS PhD
Enteral
• Feed Type
• NGT or NJ
• Gastrostomy /PEG
• Jejunostomy
• Choice of feed
•
•
•
•
Osmolarity
Caloric density
Fibre
Special formulas
Prof. Marvin Reid MB BS PhD
Enteral Tube
Feeding
Metabolic/
Physiologic
imbalance
No
Yes
Use Standard
Solution
Disturbed
Absorptive
capacity
Lactase
deficiency
Metabolic
stress
Fluid
restriction
Electrolyte
restriction
Prof. Marvin Reid
Elemental
products
Soy products
Protein rich
solution
Concentrated
Solution
Low
electrolyte
solutions
Feeding into the stomach- Gastric
Feeding Practice
• Intermittent gastric feeding
• Aspirate. Use GRV guidelines
• Start at 30 ml/h or 25% of goal of full strength
• Increase by 10 ml ever 12-24hr depending on illness
severity
• Flush with 30 ml water or Pepsi after each feeding
• Recline permitted >2hrs after feeding
Prof. Marvin Reid MB BS PhD
Use of GRV
• > 500 ml =stop & reassess patient tolerance
• >200 but <500 – may indicate intolerance –reassess
& initiate algorithmic reduction of risk
• <200 –usually indicates tolerance
Prof. Marvin Reid MB BS PhD
NJ or Jejunostomy feeding practice
• Appropriate feed
• Incline 30-45˚ during infusion
• Slow continous infusion using pump. Start at 20-30
ml/hr increase q4h by 10 ml until goal.
• Formula in bag –fridge± hang time >4 hrs
discouraged. Used Closed Enteral System if
possible.
• Flush q4h with 30 ml water
Prof. Marvin Reid MB BS PhD
Complications of Enteral
• Intolerance of enteral feed
• High GRV
• Abdominal distension & cramping
• Diarrhea (>500 ml/d)
• Complication of Enteral
•
•
•
•
Tube related
Diarrhea
Aspiration
Metabolic
Prof. Marvin Reid MB BS PhD
Reducing Aspiration
• feeding –change level (below ligament of Treitz) ±
Continuous infusion rather than intermittent± Use
smaller tubes
• Oral hygiene
• Posture –head or reverse trendeleburg at 30-45˚
• Use prokinetics
• Increase nursing staff
Prof. Marvin Reid MB BS PhD
Diarrhea
• Causes
•
•
•
•
•
Medications –antibiotics, antaacids, sorbitol in elixirs
Lactose
Infection & feed contamination
Osmolalitity of feed
Inappropriate rate or formula
Prof. Marvin Reid MB BS PhD
Medication
• Tablets crushed in 10-15 ml water
• Gelatin capsule opened and powder dissolved in
10-15 ml water
• Do not add to enteral formula
• Stop feed. Flush line. Give meds. Flush again.
Restart feed.
Prof. Marvin Reid MB BS PhD
Immunonutrition
• Benefits or enhances immune system
• Arginine conditionally essential during sepsis
• Macrophages
• Active uptake in infection
• iNOS –NO
• Arginase-metabolism of arginine to ortnithine =precursor of
proline & polyamines
• T cell proliferation
• Arginine 12g/l (4% energy) and N-3 fatty acid
1g/1000kcal –beneficial
• Modulation of antioxidant defense –selenium, GSH
Prof. Marvin Reid MB BS PhD
Effect of Immunonutrition on Mortality in 22
Trials
P value for homogeneity is .54
Heyland
et al JAMA 2001
Prof. Marvin Reid MB
BS PhD
Effect of Immunonutrition on infectious
complications in 22 Trials
P value for homogeneity is <0.001
Heyland
et al JAMA 2001
Prof. Marvin Reid MB
BS PhD
Quantity
Prof. Marvin Reid MB BS PhD
Nutritional State
Nutritional State
Demand
Requirements
Prof. Marvin Reid MB BS PhD
Energy requirements
• TDR=BMR(60-75%)+EEA(15-30%)+TER(~10%)
• BMR-amount of energy expended to maintain a
living state at rest 12-18hr after a meal
• Synonyms =BER, BEE, RMR, REE
• REE or RMR=sum of BEE , nonshivering
thermogenesis and stress hypermetabolism
• BMR and REE differ <10%
Prof. Marvin Reid MB BS PhD
Estimating EE
• Measured directly
=Direct calorimetry
• Measured indirectly
=indirect calorimetry
• Estimated from
equations eg HarrisBenedict, WHO/FAO,
Ireton-Jones
Prof. Marvin Reid MB BS PhD
Protein requirements
• Obligatory Protein loss -46-69 mg/kg not related to
age & sex
• WHO -0.75 g/kg for adults
• Physiological factors
• Life cycle=growth, preg & lactation
• Energy intake
• Pathological factors –hypermetabolism (1-2 g/kg/d)
Prof. Marvin Reid MB BS PhD
Vitamins
• Vitamins, trace elements, and electrolyte
requirements are empirical
• ? Iron in PEM & Sepsis
• ? Thiamine in ICU patients
Prof. Marvin Reid MB BS PhD
Conclusion
• Nutrition plays important role in recovery of
critically ill patients
• Enteral nutrition is the preferred route
• The practice is evolving & becoming more
sophisticated
Prof. Marvin Reid MB BS PhD
END
• Define malnutrition
• Identifying individuals at nutrition risk
• Principles of Nutrition assessment
• Administering Nutrition support
Prof. Marvin Reid MB BS PhD
Nutrition & GI
Sickle Cell Unit
Jamaica
Clinical Nutrition
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
1
Objectives


Sickle Cell Unit
Jamaica
Review of GI
Physiology
Nutritional
management of
selected GI diseases
eg




Dumping syndrome/
pancreatitis /
Short Bowel Syndrome/
Liver disease
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Amplification of the surface area of the
human small intestine
Cylinder
x1
3,300 cm2
Folds
x3
10,000
cm2
Villi
x10
100,000
Microvilli
x20
2,000,000
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Intestinal cell renewal



Sickle Cell Unit
Jamaica
Dividing mucosal cells are found near the crypt
region
Following proliferation, cells migrate to the base of
the crypt to become paneth cells or the villous
region where they become progressively
differentiated and assume various digestive and
absorptive function
Turnover =48-72hrs
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Function of Intestinal epithelium






Barrier and immune function
Fluid & electrolyte absorption
Protein synthesis
Nutrient digestion & absorption
Fluid & electrolyte secretion
Mediator production
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Fluid Flux in GIT
Sickle Cell Unit
Jamaica
Intake
~2L
Gut Secretions
~7L
Total
~9L
Absorption
Small intestine
~7.5L
Colon
~1.3L
Output
~0.2L
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Water movement



Sickle Cell Unit
Jamaica
The intestinal mucosa acts as a
semipermeable membrane (size of tight
junction)
Water movement is passive and follows solute
movement
Mucosal permeability varies along length of
intestine highest in jejenum & lowest in colon
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sodium Absorption

Na-H Exchange


Na-dependent Co-transport


Small bowel /post prandial
Coupled Na-C / Absorption


Proximal small bowel/Non-nutrient
Ileum,colon
Na Channel

Distal colon
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Sodium dependent cotransport


Na-glucose cotransporter in the luminal
membrane
Basis of ORF
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
NA Flux in GIT
Sickle Cell Unit
Jamaica
Intake
~150 mmol
Gut Secretions
~1000 mmol
Total
~1150 mmol
Absorption
Small intestine
~950 mmol
Colon
~195 mmol
Output
~5 mmol
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Potassium



Sickle Cell Unit
Jamaica
Overall K+ movement is the result of solvent
drag and is potential-dependent
Active K+ secretion occurs in the colon
Recto-sigmoid has an active K+ absorptive
process most likely K-H exchange
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Chloride

Potential-dependent Cl absorption



Sickle Cell Unit
Jamaica
Jejenum & ileum
Coupled Na and Cl absorption
HCO3 dependent Cl absorption

Ileum / colon / rectum
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
K & Cl Fluxes in GIT
K
CL
Intake
80 mmol
150
Gut
Secretions
Total
40 mmol
750
120 mmol
900
110 mmol
800
-3 mmol
97
13 mmol
3
Absorption
Small
intestine
Colon
Output
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Major areas of nutrient
absorption

Carbohydrate


Lipid/Protein


Duodenum/jejenum
Iron


Duodenum/jejenum
Duodenum
Bile salts

Ileum
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Carbohydrate absorption
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Glu transporters


Sickle Cell Unit
Jamaica
SGLT1 (Sodium-dependent glucose cotransporter) upregulated by luminal Glucose. Related to glucose
transporter in renal tubule
GLUT2 (glucose transporter)– facilitated diffusion
exit at basolateral membrane
Basolateral
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Regulated translocation of GLUT2 in food-facing enterocyte membranes.
Sickle Cell Unit
Jamaica
Leturque A et al. Am J Physiol Endocrinol Metab
2009;296:E985-E992
©2009 by American Physiological Society
Tropical Medicine Research Institute
The University of the West Indies
Fat luminal digestion &
absorption





Sickle Cell Unit
Jamaica
Emulsification by bile salts
Lipolysis –lipase
Micelle formation
Release of fatty acid & monoglycerides from
micelle and diffusion into mucosal cell.
Mucosal uptake- Binding to fatty acid binding
protein aids
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Intramucosal aspect of fat
absorption



Sickle Cell Unit
Jamaica
Re-esterification –cytoplasmic carrier proteins
to Smooth endoplasmic reticulum (sER)
Chylomicron & VLDL formation
Secretion- into intestinal lacteals
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Medium Chain Triglycerides




Sickle Cell Unit
Jamaica
8-10 carbons
Micellar formation not required
No reesterification in mucosal cell
Transported in the portal blood as free fatty
acid
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Protein digestion & absorption



Sickle Cell Unit
Jamaica
Pancreatic proteolytic enzymes break
proteins into oligopeptides and AA
Brush border peptidases hydrolyze
oligopeptides into di and tri peptides
Di and tripeptides are absorbed across
mucosal cells
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Peptide & AA absorption
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Defects asociated with
Malabsorption




Impairment of mechanical digestion
Impairment of chemical digestion
Impairment of solubilization
Anatomic/Pathologic impairment of
absorption
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Conclusion

Sickle Cell Unit
Jamaica
The GIT is very active metabolic organ that is
adapted for its role in digestion & absorption
of nutrients.
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Dumping Syndrome


Sickle Cell Unit
Jamaica
Pyloric sphincter bypass
Symptoms –


Early during a meal or within 30 minutes
Late ~ 3hrs after a meal









Nausea
Vomiting
Abdominal pain, cramps
Diarrhea
Dizziness, lightheadedness
Bloating, belching
Fatigue
Heart palpitations, rapid heart rate
Hypoglycaemia & mental confusion may occur as late symptoms
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
enteroglucagon, peptide YY, pancreatic
polypeptide, vasoactive intestinal polypeptide,
glucagonlike peptide-1 (GLP-1), neurotensin,
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Nutrition Therapy



Sickle Cell Unit
Jamaica
Limit simple sugars
Emphasize high protein high fat foods
Eat small frequent meals
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Pancreatitis


Sickle Cell Unit
Jamaica
Mild pancreatitis - Usually self-limiting ;
Nutrition appears not to affect clinical
outcome; Enteral nutrition tolerated and may
be associated with less adverse effects.
Severe pancreatitis - TPN is preferred
especially if fistula develops. Lipid safe
provided baseline TG results normal
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Severe Pancreatitis




Sickle Cell Unit
Jamaica
Chronic Pancreatitis
20 -30% develop DM
pancreatic exocrine insufficiency lipase(<10%) + tyrpsin
Low fat diet, MCT, pancreatic enzymes, H2Blockers,antibiotics if Small Bowel Overgrowth
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Short Bowel Syndrome

Sickle Cell Unit
Jamaica
Clinical syndrome produced by loss of
mucosal absorptive area and shortened
intestinal transit time due to resection.

diarrhoea, wt loss, malnutrition, steatorrhea.
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Short Bowel Syndrome

The effect is dependent upon





site of resected bowel
whether both ileum and colon resected
extent of resection
functional capabilities of remaining bowel
adaptation of remaining bowel
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Sickle Cell Unit
Jamaica
Short Bowel Syndrome


Sickle Cell Unit
Jamaica
Patients with jejunostomy and <100 cm of
jejunum usually require permanent TPN
Patients with intact colon and <50 cm of
jejunum usually require permanent TPN
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
SBS-Management Principles




Sickle Cell Unit
Jamaica
<30% resection with colon-usually no significant
nutritional effect;low oxolate diet;vit B12
30-50% resection with colon- fat restricted, low
oxolate; enteral therapy
>50% resection with colectomy - TPN initially;
enteral intake 50-100% expected goals. elemental
diet vs polymeric diets
>75% -TPN
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Malnutrition in cirrhosis
Sickle Cell Unit
Jamaica
Decrease in oral intake:
 Anorexia, nausea, vomiting, early satiety, taste
abnormalities,alcohol abuse, iatrogenic due to restrictive
diets or NPO status, medications
 Maldigestion and malabsorption:
 Fat malabsorption due to cholestasis or chronic
pancreatitis.
 Water-soluble vitamin malabsorption due to alcohol
abuse.
 Calcium- and lipid-soluble vitamin malabsorption due to
cholestasis.
 Metabolic abnormalities:
 Glucose intolerance, increased protein and lipid
catabolism
similar
to sepsis, trauma or other catabolic
Tropical Medicine
Research
Institute
Dr. Marvin Reid MB BS PhD
states.
The University
of the West Indies

Liver Disease
Sickle Cell Unit
Jamaica
Protein
Energy goal
Hepatitis
1-1.5
30
Prevent malnutrition
Cirrhosis
1-1.5
30
Prevent malnutrition
Treat fat malabsorption
30
Provide nutritional needs
without encephalopathy
Encephalopathy 0.5-0.75
Tropical Medicine Research Institute
The University of the West Indies
Dr. Marvin Reid MB BS PhD
Severe Childhood Undernutrition
Dr. Carolyn Taylor-Bryan
Objectives
• Definitions
• Classification
• Clinical features
• Principles of management
• Prevention
Human nutrition
• The process by which humans obtain food and
use it for growth, metabolism, and repair
Food
intake
Metabolic
demand
Mismatch between supply & demand leads
to alteration in form & function
= MALNUTRITION
Malnutrition
• Primary
- results from inadequate dietary intake
- no underlying illness
• Secondary
- accompanies any disease which disturbs
appetite, digestion, absorption or utilization of
nutrients
Primary Malnutrition
• Dependent and vulnerable - rely on others for
nourishment
• Young child, elderly, prisoners, mentally
subnormal
Causes of malnutrition
• Social factors
• Economic factors
• Biologic factors
• Environmental factors
Classification of Malnutrition
Classification of Malnutrition
•
Gomez
•
Wellcome
•
Waterlow
•
WHO
Wellcome Classification
Children were grouped according to 2 criteria:-
• The presence or absence of edema
• Weight deficit of the child for his/her age
Wellcome Classification
Wt for age (%)
Edema absent
Edema present
60-80
Undernutrition
Kwashiorkor
<60
Marasmus
Marasmickwashiorkor
* Modified Wellcome
> 80% wt /age + edema – edematous malnutrition
Waterlow Classification
Wt for Ht deficit Ht for age
deficit (%)
(%)
Normal
90-120
95-110
Mild
Moderate
Severe
80-89
70-79
<70
90-94
85-89
<85
Waterlow Classification
• Wasted child
- immediate clinical problem where rehabilitation
can lead to restoration of the lost tissue
• Stunted child
- likely to depend upon public health measures
aimed at environmental improvement
WHO
http://www.who.int/ nut/documents/manage_severe_malnutrition_eng.pdf
Criteria
Moderate
Severe
Oedema
No
Yes
Wt / Ht
-3 <SD Score <-2
(70-79%)
< -3 SD Score
(<70%)
Ht/age
-3 <SD Score <-2
(85-89%)
< -3 SD Score
(<85%)
For children >6 mo weight for height 1 z score unit is nearly equal to 10% median.
For >6 mo Height for age 1 z score unit is nearly equal to 5 % median.
http://www.who.int/nutrition/publications/guidelines/
updates_management_SAM_infantandchildren/
en/
• MUAC <11.5cm
• Wt/ht < -3 z-score
• Bilateral edema
Management of Severe
Malnutrition
Aims of treatment
• Feed the patient so that weight is gained at an
accelerated rate and ‘catches up’ with normal
• Stimulate mental development
• Protect patient from relapse
• Secure a continued normal development after
discharge
History taking
Case - 8 month old male
• Exclusively breastfed until 6 months of age at
which time he developed a skin rash
• Taken to the doctor
• Dx with eczema
• Mother told not to give baby cow’s milk formula
and coincidentally at this time infant refused
breastmilk
Case – 7 week old female
• Mother 16yo
• Breastfeeding unsuccessful
• Enfamil / Lactogen given in first week of life – did
not take it well
• “Marigold” bush tea only since 1 week of life
Case - 6 month old male
• 5 am…… 2oz bush tea with sugar
• Day ……. 3 servings/d 4oz cornmeal porridge OR
Nestum + Lasco food drink / formula OR
formula only
• 6pm – 5am….. 3 servings bush tea
1 large tin formula / month
Clinical Assessment - history
Presenting history
- V & D - ? dehydration
- RTI
Perinatal history
- birth weight
Past medical history
- admissions
- known illnesses
- allergies
Clinical Assessment - history
Immunization
Developmental history
Family history
- age parents / primary caregiver
- occupation parents
- level of schooling of parents
- number of siblings - family tree
- ? contraception
Clinical Assessment - history
Social history
- caretaker of patient
- provider of financial support
- average income/week
- details of housing / amenities
Clinical Assessment - history
Dietary history
- breastfeeding history
- formula
- other milk feeds
- porridge / cereals
- mixed diet
- teas
- juices
- bag snacks
- typical recall of meals / day
Clinical Assessment - history
• This information useful in establishing whether a
nutrient deficiency is primary or secondary
Examination of the patient
Clinical Assessment – Examination
Marasmus
•
•
•
•
•
•
Apathetic
Generalized muscular wasting
Absence of subcutaneous fat
‘skin and bones’ appearance
Hair – sparse, thin, dry, loss of sheen
Old person’s face – sunken cheeks due to
disappearance of fat pads
• ± abdominal distension
• Skin – dry, thin, wrinkles easily
Clinical Assessment – Examination
Kwashiorkor
•
•
•
•
•
•
Apathetic & irritable
Pitting, painless edema
Dermatitis
Hair changes
± abdominal distension
Hepatomegaly
Clinical Assessment – Examination
Marasmic-Kwashiorkor
• Combines clinical characteristics of kwashiorkor
and marasmus
• Edema ± skin lesions (kwashiorkor)
• Muscle wasting & decreased s.c fat (marasmus)
Clinical Assessment – Examination
Anthropometry
•
•
•
•
•
•
Weight
Height
Head circumference
% wt/age
% ht/age
% wt/ht
Clinical Assessment – Examination
Altered affect
• apathetic
• irritable
Cry
Wasting :severity
Pitting edema :severity – feet, legs, thighs,
sacrum, hands, periorbital
Clinical Assessment – Examination
Edema
• Pitting
• Dependent
• Severe cases - entire body & internal organs
may be edematous
Clinical Assessment – Examination
Wasting
• Prominent ribs & limb joints
• Redundant skin folds –axillary, gluteal
• Winging of scapula
Clinical Assessment – Examination
Hair
Scalp
• dull, dry, thin, fine, sparse, bald
• atrophy of hair roots – easily & painlessly
pluckable
• forest sign / flag sign
Eyelashes - long & luxuriant, colour change
Eyebrows – lost, colour change
Excess growth of lanugo hair
Clinical Assessment – Examination
Eyes
•
•
•
•
•
Pale conjunctiva
Angular palpebritis
Corneal & conjunctival xerosis
Bitot’s spots
Jaundice
Clinical Assessment – Examination
Cheeks
• Jowls – fullness associated with edematous
malnutrition –also seen in marasmus
• Cause unknown
Clinical Assessment – Examination
Mouth
•
•
•
•
•
•
Angular stomatitis
Oral candidiasis
Atrophic tonsils
Tongue – hyperaemic, swollen, smooth, sores
Teeth – missing or erupting abnormally, cavities
Gums – bleeds easily, recession of gums
Clinical Assessment – Examination
Abdomen
• Distended – gaseous distension secondary to
bacterial overgrowth
• Hepatomegaly –smooth, firm, non-tender triglyceride accumulation
Clinical Assessment – Examination
Skin
• Sequential changes
• Becomes darker espc over pressure areas &
places exposed to minor trauma
• Drying & cracking of superficial skin revealing
pale areas between the cracks (crazy pavement
dermatosis)
• Dry cracked layer then peels off leaving thin
hypopigmented skin (flaky paint dermatosis)
Clinical Assessment – Examination
Skin
• Skin friable
• Ulceration/ maceration -perineum, flexures,
behind ears
• Severe cases – sunburn
• Petechiae
Clinical Assessment – Examination
Bone
• Enlargement of costochondral junction –rickety
rosary (vit D, vit C, copper, phosphate
deficiency)
• Craniotabes
• Frontal & parietal bossing
• Persistently open anterior fontanelle
• Knock-knees, bow-legs
• X-ray – marked osteopenia
Clinical Assessment – Examination
Neurologic
• ‘Kwashi shakes’- Parkinsonian-like tremors in
recovery phase (transient)
Clinical Assessment – Examination
Palms
• Pallor
Reduced intake
↓ body mass
•
Reduced requirements
• Relative reduction in
requirements
- efficient use
- reduced work
Body composition
changes
Physiological & metabolic
changes
Loss of reserve tissue & functional capacity
Loss of homeostasis
Treatment regimes must always work within the
patient’s limited metabolic capacity…….
whilst the reductive adaptations are reversed
dietetically
Investigations
•
•
•
•
•
•
•
•
CBC, diff, film, Hb electrophoresis
Urea & electrolytes, LFTs,
VDRL, HIV
Blood culture, urine culture
Urineanalysis
CXR
Stool – ocp, culture
Other tests as indicated
Treatment
• Resuscitative / maintenance (1-2 wks)
• Rapid catch up phase / rehabilitation
(4-6wks)
• Preparation for home (1-2wks)
• Follow-up after discharge
Resuscitative phase
Aim
• Resuscitate patient – treat infections
- restore electrolyte balance
• Dietary management
- give enough to prevent hypoglycemia and hypothermia,
to prevent further tissue catabolism and allow for
reversal of physiological changes without overloading
the limited capacity of the heart, kidney, intestine or liver
Resuscitative phase
• Treat or prevent dehydration (± vomiting &
diarrhea)
- oral route preferred
- iv fluids only if there are definite signs
of shock
Resuscitative phase
• Treat infections
- broad spectrum antibiotics -10 days
- first line treatment – amoxil, gentamycin,
flagyl
- if fail to improve within 48 hrs / deteriorates –
switch to second line therapy – cephalosporin &
amikacin
Resuscitative phase
• Other infections
- staphylococcus skin infection – cloxacillin
- oral candidiasis – nystatin suspension
- groin candidiasis – antifungal cream
Resuscitative phase
• Replete specific nutrient deficiencies
- give adequate amounts of vitamins – tropovite,
folic acid
- mineral mix (PotMgCitZn)
- iron not given in this phase
Resuscitative phase
• Start to feed the child
- reverse physiological changes
- prevention of further tissue catabolism
- feed frequently and in small amounts (not
> 4hrly)
energy 80-100 kcal/kg/d
protein
0.8-1.2 g/kg/d
Resuscitative phase
• Identify and treat other problems
- hypothermia
- anemia
End of resuscitative phase
• Treatment of infection
• Loss of edema
• Return of appetite
• Return of affect
Rehabilitation
• Aim -to encourage the child to eat as much as
possible to gain as much weight in the shortest
time period
• The energy density of the feed is increased by
adding a concentrated source of calories to the
diet
Rehabilitation
• FeSO4 added
• Daily weights plotted on a graph
• Encouraged to complete feeds
• Feeds increased daily at TMRU until child fails to
complete feeds
• Can be allowed out of crib for playtime – risk of
cross infection is less, minimize delay in mental
Rehabilitation
• End of RCUP marked by plateau –usually
between 90-110% of expected weight for height
Growth Curve
Preparation for home
• Switched to age appropriate diet
• May lose weight initially as food is often refused
• Once established on diet – for home
• Mothers to be encouraged to come often –
participate in bathing, feeding child
• Stimulation – toys in crib, play stimulation daily,
bright pictures on the ward
Preparation for home
Weekly workshops for parents
• Malnourished Children Foundation
• Parenting, safe practices, nutritional advice,
stimulation
• Decrease risk of recurrence
Preparation for home
• Social worker reports on home situation before
discharge
Follow up
• Followed up post discharge
Prevention
Target at risk victims
- children <2y.o.,
- parents who have misconceptions concerning the
use of foods
- low socioeconomic strata
- unstable families
- poor sanitary conditions
Take home points
Initial evaluation of all children
………..NUTRITION SCREEN
• Weight
• Weight change
• Height
• Nutritional hx
Take home points
In resuscitation phase
- feed to appetite / don’t force feed
- no high protein, high calorie diet
- don’t chase electrolytes
- avoid iv fluids
- antibiotics i.m.
- fever – sponge & fan therapy….NO panadol
Reading material
• Oxford Textbook of Medicine 2nd Ed, Ed Weatherall et
al, pp 8.12-8.21, 1986
http://www.who.int/ nut/documents/manage_severe_malnutrition_eng.pdf
Thank You
NUTRITION CONCEPTS AND APPLICATIONS IN MEDICINE
MALNUTRITION
and
DEMAND FOR ENERGY
Sept 2020
Focus
• Malnutrition as an imbalance between the demand
and supply of energy to meet the body’s
requirement
• Methods used to measure energy requirements
• Nutrition is a demand led process
– varying throughout the life cycle from in utero to
the elderly
– varying with different physiological and
pathological states
• Primarily the demand is for energy
• The DEMAND represents energy required to:
– to support the synthetic activities of the body
– to fuel the metabolic processes of the body
• leading to expended energy as heat
Energy requirements of healthy individuals
Definition by FAO/WHO/UNU 2004
is the amount of food energy needed to balance energy expenditure
in order to maintain:
– body size
– body composition
– at a level of necessary and desirable physical activity
– all consistent with long-term good health.
• Includes energy for
– the optimal growth and development of children
– the deposition of tissues during pregnancy, and the secretion
of milk during lactation consistent with the good health of
mother and child.
How the demand/requirement for energy
may be satisfied?
• CHO, lipids, proteins (and alcohol) provide all the
energy supplied by foods
• CHO, lipids & proteins are macronutrients
• in contrast to vitamins and minerals often referred
to as micronutrients
• Energy is NOT a nutrient
Gross energy to metabolisable energy
Gross energy
kcal/g
CHO Fat Pro
4.10 9.45 5.65
Faecal energy
loss
1 cal = 4.18 J
Alcohol: 7 kcal/g
Digestible energy
kcal/g
CHO Fat Pro
4.0 9.0 5.2
Atwater factors
urinary energy
loss as N
Metabolizable energy
kcal/g
CHO Fat Pro
4.0 9.0 4.0
Acceptable Macronutrient Distribution (AMD)
Range
for normal children and adults
(% of total calories)
CHO
FAT
PROTEIN
Children
1- 3 y
45 - 65
30 - 40
5 - 20
Children
4 -18 y
45 - 64
25 - 35
10 - 30
Adult
45 - 65
20 - 35
10 - 35
Saturated fat < 10% to reduce cardiovascular disease*
Added free sugar < 5% ( no more than 10%)

*Institute of medicine (IOM), 2006
Calculation.1
• If total energy intake in an adult = 2500 kcal
• fat intake is 135g, protein intake is 65g, added
free sugar is 150g
• % Energy derived from fat =
• 135 x 9/2500 x 100 = 49%
• High fat intake
• % energy from protein =
• 65 x 4/2500 x 100 = 10%
• Within normal range
Comments?
Calculation.2
• % Energy derived from added free sugar =
• 150 x 4/2500 x 100 = 24%
• High intake
• Associated with obesity and NCDs
• Global guidelines Limiting sugar consumption < 10%
- (preferably less than 5%)
• Include guidelines from:
–
–
–
–
–
WHO
World cancer research
International Diabetes Federation
US Academy of Medicine
others
Energy balance
Essential in assessment of energy requirement
• Components of energy balance:
– energy intake
– energy expenditure
– energy stores
positive
Energy Balance
Energy
intake
Energy
expenditure
negative
1. Equilibrium/balance: energy intake = energy
expenditure
 maintaining weight (no change in energy stores)
 according to 1st law of thermodynamics
2. Negative energy balance: intake < expenditure
 weight loss
 underfeeding or starvation may lead to:
 wasting: weight-for-length or height less than reference
 stunting: Length or height-for-age less than reference
• 3. Positive energy balance:
intake > expenditure
– increase in energy stores:
• growth, pregnancy
• recovering weight loss eg from illness
• development of obesity
• Only ~10 kcal/d in excess to gain 1 lb/year
(3500kcal)
Estimated ~925 million malnourished people in the world
(WHO, 2010)
Children
• Globally, 165 million children under five are estimated to
have low length/height-for-age (stunting)
• more than 100 million have low weight-for-height (wasting)
• Undernutrition is associated with ~ 45 % of death in children
under 5 years of age
• 43 million are overweight or obese.
Adults
• obesity is a global health problem
• huge health and economic cost
Ref: MOHW-National strategic and action plan for the prevention and control of noncommunicable diseases in Jamaica 2013 - 2018
Majority of children have same potential to grow: but cannot
reach genetic potential without adequate Energy and nutrients
Same age
Globally, 1 in 4 children is stunted
associated with lower adult cognition, educational attainment, and
income. (2013 lancet series)
Estimating energy requirements in
healthy population
Energy requirements of healthy individuals
Definition by FAO/WHO/UNU 2004
is the amount of food energy needed to balance
energy expenditure in order to maintain:
–
–
–
–
body size
body composition (fat and lean)
at a level of necessary and desirable physical activity
all consistent with long-term good health.
• Includes energy for
– the optimal growth and development of children
– the deposition of tissues during pregnancy, and the secretion
of milk during lactation consistent with the good health of
mother and child.
Estimating normal energy requirements
• In theory energy requirements could be based on
measurement of:
– either energy intake
– or energy expenditure
– or both
• Measurement of dietary intake is usually less reliable than
measurements of energy expenditure
• WHO recommends measuring energy expenditure using
the Double labelled Water (DLW) method and/or minute-byminute heart rate monitoring for estimating total energy
requirements
- basis of WHO Human Energy requirements (2004)
Human energy requirements
Report of a Joint FAO/WHO/UNU
Expert Consultation, 2004
Free online
Theoretical concept of measuring energy
expenditure
• To produce energy in the body, macronutrients are
oxidized or combusted in the presence of oxygen to
release carbon dioxide, water and heat.
• The heat/ energy produced can be measured:
– directly in a whole body calorimeter
– or estimated indirectly from O2 consumption and CO2
production ( respiratory exchange using indirect calorimetry)
Techniques for measuring energy
expenditure.
Generally based on:
1. Direct calorimetry
2. Indirect calorimetry
DIRECT CALORIMETRY
• Direct measurement of
– heat produced by a subject placed in an enclosed
structure large enough to permit moderate activity
• Limitations
– confined nature of testing conditions
– technically demanding
– high cost
– infrequently used
INDIRECT CALORIMETRY
• Frequently used
• Indirect assessment of heat/energy
• by respiratory gas analysis:
from measuring O2 consumption and CO2
production in breath
• Based on the fact that:
When components of the macronutrients ( glucose,
fatty acids and amino acids) are oxidized in the body
to produce energy, O2 is used and CO2 is produced in
proportion to the heat generated as illustrated with
glucose
Concept of indirect calorimetry.1
A simple example is combustion/oxidation of glucose:
C6H12O6 + 6O2 =
180g
6 x 22.4
liters
6CO2 + 6H2O + heat
6 x 22.4
liters
6 x 18g
Can be
measured
directly or
indirectly
2.78 MJ
Therefore for CHO,
1 litre O2 consumption = 2.78/(6 x 22.4) = 20.8 kJ or 4.95 kcal
Similarly,
1 litre CO2 produced = 2.78/(6x22.4) = 4.95 kcal expended
Concept of indirect calorimetry. 2
Similar equations for the combustion of fatty acids and
amino acids:fatty acid:
4.60 kcal/liter O2 consumed
amino acids:
4.49 kcal/liter O2 consumed
glucose:
4.95 kcal/liter O2 consumed
• The values are fairly close, so an average of 4.8 kcal/liter
O2 consumed is commonly used to calculate Energy
production of mixed foods from O2 consumption.
• Similar application for CO2 production
• Sometimes both O2 consumption and CO2 production used
 Respiratory quotient (RQ)
= moles CO2 expired/ moles O2 consumed
 depends on nutrient mixture




CHO = 1
FAT = 0.7
PROTEIN = 0.8
Typical western diet = 0.87
 Gives an idea of fuel or substrate (CHO,
fat, protein) utilization
COMPONENTS OF TOTAL ENERGY EXPENDITURE
Components of total energy expenditure (TEE):
– BMR + Physical activity energy expenditure + diet induced
thermogenesis (DIT)
BMR (Basal metabolic rate or basal energy expenditure)
– It is the minimum level of energy expended by the body to
sustain life in the awake state
1. membrane function, eg ionic movement
2. substrate turnover, eg protein turnover
3. mechanical work
– Usually the largest component of TEE (~45 -70%)
– relatively constant within a normal individual over time
– determined mainly by the individual’s age, gender, body
PHYSICAL ACTIVITY
• Physical activity energy expenditure (PAEE)
accounts for ~15 to 30 % of TEE in most
individuals
• Most variable component of energy
expenditure
Diet induced thermogenesis (DIT) or
thermic effect of food (TEF)
Energy expended to digest, metabolize, convert and
store ingested macronutrients
- extends over at least 5 h.
~ 10% of the BMR over a 24-hour period in
individuals eating a mixed diet
So, methods for measuring energy expenditure
may be based on:
• direct measure of total energy expenditure
• or measuring components of energy
expenditure
Equipment for INDIRECT CALORIMETRY
• Respiratory gas analysis can be achieved
– over short measurement periods at rest
– during exercise using a face mask, mouthpiece or canopy
– or over longer periods using large respiration chamber
Limitations
– Hyperventilation may occur in subjects who are not well
adapted to a mouthpiece
– Difficult to obtain an airtight seal with mouthpiece
– Environment in respiration chamber is artificial
Respiration chamber- attached to O2 and CO2 sensors
Equipment for INDIRECT CALORIMETRY contd
• The ventilated canopy system- for RMR
MEASUREMENT OF BMR
• BMR is measured under standardized conditionsafter;
– ~12h fast
– while resting comfortably, supine, awake and
motionless
– in a thermoneutral quiet environment.
• Difficulty in achieving BMR under most
measurement conditions, so RMR or REE is
frequently measured using the same conditions
(~ 3% difference)
BMR PREDICTIVE EQUATIONS #1
Harris-Benedict ( kcal/d)
• Men
– BMR = 66 + (13.7 x weight in kg) + ( 5 x height in cm ) - (6.76 x
age in years )
• Women
– BMR = 655 + (9.6 x weight in kg) + (1.8 x height in cm) - (4.7 x
age in years)
• Other equations:
– Schofield for adults
– Cunningham for adults
– FAO/WHO/UNU 1985 for children and adults
MEASURMENT OF FREE LIVING PHYSICAL ACTIVITY
ENERGY EXPENDITURE (PAEE)
METHODS
1.
2.
3.
4.
5.
Heart rate recording monitor
Various motion detector devices - accelerometry
Observer record of time and motion of activity
Activity diary
Derived from estimates of TEE , BMR & TEF
TEE = BMR+ PAEE+ TEF
PAEE = TEE- (RMR + TEF)
Most accurate when TEE is measured accurately by the
doubly labelled water
DOUBLY LABELLED WATER (DLW)
isotopic technique
• Most substantial advance in the measurement of Total
Energy Expenditure in humans living under their
habitual free living conditions
– using stable isotopes to trace water kinetics and to determine
CO2 production- how?
• A bolus oral dose of two isotopic water is given:
1. 2H2O – water isotopically labeled with 2H (deuterium)
2. H218O - water isotopically labeled with 18O
• Urine or saliva or plasma samples are collected over
about 7 – 14 days
• for isotopic analysis using Mass-spectrometry
• the rates of elimination of the isotopes are calculated
DOUBLY LABELLED WATER (DLW)
isotopic technique
• the rate of CO2 production is derived from rates of elimination of
the isotopes
• Hydrogen in body water is eliminated only as water.
• Oxygen in body water is eliminated as both water and CO2
• The difference between the elimination rates of the two isotopes
represents CO2 production.
DOUBLY LABELLED WATER (DLW)
isotopic technique
• CO2 production is the result of fat, CHO and protein oxidation ie
index of energy expenditure
• is equated to energy expenditure using indirect calorimetric
equations.
DOUBLY LABELLED WATER
Advantages
Non invasive, unobtrusive
Disadvantages
Limited availability
Performed under free living
conditions
Expensive
Performed over several days
Can be used to derive activity
energy expenditure ( best estimate)
TEE = REE + Activity EE + TEF
Reliance on Isotope ratio
mass- spectrometer
HEART RATE RECORDING
• Usually based on correlation between heart rate
and oxygen consumption during moderate to heavy
exercise
• The correlation is poor at low levels of physical
activity
• When used to estimate energy requirements,
individual calibrations of the relationship
between heart rate and oxygen consumption
are done.
ENERGY REQUIREMENT: eg factorial calculation
Energy requirement of a male engaged in heavy work: age
35 y, wt = 65 kg, height = 1.72m, BMI 22
– BMR = 68 kcal/h (measured or derived)
PAR
hours kcal
In bed
1.0
8
544
Occupational activities
3.8
8
2067
Discretional (social & household) 3.0
activities and leisure
1
204
For residual time
Bathing, dressing etc
7
666
Total
1.4
(RMR x PAR x hrs)
3481
PAR: physical activity ratio expressed as multiple of RMR
Physical activity level- PAL
PAL = TEE/REE
Used in classification of lifestyle
• Sedentary or light activity lifestyle: 1.40-1.69
• Active or moderately active lifestyle: 1.70-1.99
• Vigorous or vigorously active lifestyle: 2.00-2.40
Ref: WHO
How might pathology alter the demand for energy ?
examples
Change in Basal energy expenditure
Large increase in hypermetabolic states
Other metabolic states
• Eg
– Hyperthyroidism: weight loss
– Hypothyroidism: weight gain
– HBSS: hypermetabolic state eg:
 Increased bone marrow activity
 higher red cell turnover
 higher protein turnover
Nutritional support: severe undernutrition
• A main objective of nutritional support
– is to ensure that all interventions are within the
functional capacity of the individual ie metabolic
demand
– to prevent further metabolic stress on the brittle
homeostatic system
• Possible danger of over enthusiastic nutrition support
– can project an individual from a situation of just
being able to cope to one of being unable to cope
Nutritional support: severe undernutrition
• During acute resuscitation, problems such:
– infection, dehydration, oedema, electrolyte and
micronutrient deficiencies are treated
• During this time a diet providing energy and protein
enough to maintain body weight is given
– ie within functional capacity & matching demand
– 80 -100 kcal/kg/d (WHO, 2007)
– ~0.7 -1 g protein/kg/d
Nutritional support: severe undernutrition
Catch-up growth (protein-energy relationship)
• When the acute problems have been treated and
appetite and affect have returned, a high energy diet
may be given for rapid catch-up growth (RCUG)
• % energy derived from protein is important for
optimum tissue deposition during RCUG
– if < 7 % - deposition of more fat than lean tissue
– about ~11% is recommended
– because a greater increase in protein than for
energy is required to make desirable body
composition at rapid rates of weight gain
– Recommended energy intake for normal healthy
individuals are published by various export groups by
age, sex and activity level such as:
• RDA (Recommended Daily Allowance) by WHO
• DRI (Dietary Reference Intake) by Institute of Medicine
(IOM)
• Reviewed periodically
– References:
• Human energy requirements , UNU/WHO/FAO, 2004
• Dietary Reference Intakes for Energy, Carbohydrate, Fiber,
Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids
(Macronutrients), IOM, 2005
Human energy requirements
Report of a Joint FAO/WHO/UNU
Expert Consultation, 2004
END
QUESTIONS??
Additional slides
Role of protein quantity and quality in
protein/energy relationship
 Dietary Protein Quality is a measure of the:
 availability of the essential amino acids
 and utilization of amino acids
 therefore depends on aa composition & digestibility
• Essential amino acids are not made in the body and must be
provided in the diet: val, ise, leu, met, phe, lys, thr, trp in
adults. Plus arg in children
• Body cannot synthesize adequate lean tissue with insufficient
protein
– dietary energy partition to make adipose tissue
– leading to reduced bone growth and stunting
PRIMARY MALNUTRITION
Inadequate nutrition (energy and nutrients) leading to wasting & stunting
• significant wasting and/or oedema
– severe: weight-for-length/height < -3SD or MUAC < 110 mm in
children 6 to 59 months of age
– moderate: between -2SD and -3SD
– Mild: between -1SD and -2SD
• often with concurrent infective illness
• with or without stunting
• Similar SD categories for stunting using length or height-for-age
• Ref: WHO growth chart- free software online, most recent
• NB: Use length if under 2 years of age and height if older
BMR PREDICTIVE EQUATION #2
Schofield equation for adults
Males (kcal/d):
• 10 - 17 years BMR = 17.7 x W + 657
• 18 - 29 years BMR = 15.1 x W + 692
• 30 - 59 years BMR = 11.5 x W + 873
Women (kcal/d):
• 10 - 17 years BMR = 13.4 x W + 692
• 18 - 29 years BMR = 14.8 x W + 487
• 30 - 59 years BMR = 8.3 x W + 846
• W = body weight in kg
BMR PREDICTIVE EQUATIONS # 3
Energy & protein requirements FAO/WHO/UNU 1985
Age range (yrs)
BMR (kcal/d)
Males
BMR (kcal/d)
Females
0-3
60.9 W - 54
61.0 W - 51
3 - 10
22.7 W + 495
22.5 W + 499
10 - 18
17.5 W + 651
12.2 W + 746
18 -30
15.3 W + 679
14.7 W + 496
30 - 60
11.6 W + 879
8.7 W + 829
> 60
13.5 W + 487
10.5 W + 596
W = body wt in
kg
PREGNANCY
Dietary intake during pregnancy must provide the
energy that will ensure:
• full-term delivery of a healthy newborn baby of adequate
size and appropriate body composition
• by a woman whose weight, body composition and physical
activity level are consistent with long-term good health and
well-being
• ideally a woman should enter pregnancy at a normal weight
and with good nutritional status.
The energy cost of pregnancy is determined by
the energy needed:
• for maternal gestational weight gain
– which is associated with protein and fat
accretion in maternal, foetal and placental
tissues
• and by the increase in energy expenditure
associated with basal metabolism and
physical activity
• Muscle and the major organs of the body predominantly
account for RMR
– fat free mass (FFM) explains 60 – 80% of interindividual variation
– depends on composition of FFM
eg in an adult skeletal muscle: 22- 36% of RMR, brain: 20 -24%)
• RMR:
– falls with age
– is higher in males compared to females
– is higher in more active individuals than inactive
– affected by thyroid hormones (high levels increase metabolic
rate and vice versa)
• A portion of interindividual variation has been ascribed to genetic
factors- but specific source not identified
Effect on illness on energy requirements
Overall metabolic demands are not always elevated
BMR
Elevated demand: Raised BMR with illness
Reduced demand : Raised BMR with illness
PA
PA
Low
PA
Nutrition in Pregnancy and
Infancy
Dr Debbie Thompson
MBBS, Dip. Derm, PhD (Nutrition)
Objectives
1. Importance of periconceptional nutrition
2. Impact of maternal nutrition on early fetal
development
3. Role of the placenta in fetal nutrition
4. Effect of pregnancy on nutritional requirements
5. Dietary and weight gain recommendations
Importance of periconceptional
nutrition
Nutrition in Pregnancy
1. Importance of periconceptional nutrition
2. Impact of maternal nutrition on early fetal
development
3. Role of the placenta in fetal nutrition
4. Effect of pregnancy on nutritional requirements
5. Dietary and weight gain recommendations
Impact of maternal nutrition on
early fetal development
• Critical periods impact fetal development
▫ Periods of rapid cell activity/ division are particularly
vulnerable to nutritional deficiencies, toxins, and other
insults
 Famine associated with a high cumulative incidence
of heart disease
 Inadequate iron during early pregnancy associated
with poor cognitive development
▫ Metabolic or fetal programming may be able to
alter how genes are expressed during critical periods
of development
Critical Periods of Development
Figure 17.3
Nutrition in Pregnancy - Fetal
Growth
 Trimester 1 (0-13 weeks)– organogenesis
 End Trim 1: 90mm, 60g
 Trimester 2 (14-26) & trimester 3 (27-40 weeks)
- enlargement of organs and tissue
stores
 End Trim 2: 325mm, 900g
 End Trim 3: 500mm, 3200g
• Effects of malnutrition at a critical
period are irreversible
Nutrition in Pregnancy
1. Importance of periconceptional nutrition
2. Impact of maternal nutrition on early fetal
development
3. Role of the placenta in fetal nutrition
4. Effect of pregnancy on nutritional requirements
5. Dietary and weight gain recommendations
Role of the placenta in fetal nutrition
At first, nutrients are provided to the
fetus by chorionic fluid, later via
placenta:
i. In first few weeks all nutrients are
secreted by chorion into chorionic sac
which envelopes the embryo
ii. Glucose, amino acids and vitamins
absorbed by fetus’ yolk sac
iii. End Trim 1 marks transition from
yolk sac to placenta
Role of the placenta in fetal nutrition
Trimesters 2 & 3
▫ Fetus derives nutrition from placenta which:
1. Produces hormones
 Trophoblast – hCG, hPL, Prolactin
2. Exchanges gases
 O2, CO2
3. Transfers nutrients
 Placental membrane separates maternal intervillous
space from fetal blood
Fetal “supply line”
Nutrition in Pregnancy
1. Importance of periconceptional nutrition
2. Impact of maternal nutrition on early fetal
development
3. Role of the placenta in fetal nutrition
4. Effect of pregnancy on nutritional
requirements
5. Dietary and weight gain recommendations
Nutrition in Pregnancy
ADVICE TO PRE-PREGNANT WOMEN
• Optimize BMI (25 kg/m2). Obesity and overweight
are associated with infertility, pregnancy
complications, potential birth defects.
Underweight women are at risk of delivering low
BW or SGA babies
• Optimize dietary intake, removing toxic habits
• Exercise
• Manage chronic conditions
*More than 50% pregnancies are unplanned,
therefore…secure nutrition status of all
Nutrition in Pregnancy
Critical nutrient needs in critical windows
 Periconceptional through end Trimester 1
▫ Folate
▫ B12
▫ B6
▫ Kilocalorie needs are not significantly increased during the
first trimester
▫ Focus should be on intake of nutrient-dense foods
▫ A prenatal supplement is necessary
▫ Vegetarians/ vegans should be mindful of meeting needs
for essential fatty acids and vitamin B 12
▫ Drink milk to meet needs for calcium and vitamin D
Nutrition in Pregnancy
Critical nutrient needs in critical windows
 Trimester 1 - Trimester 3
▫ Vitamins
▫ Minerals
▫ Trace Elements
▫ Energy (Protein, CHO, Fats)
• Avoid foodborne illness
▫ Listeria monocytogenes- miscarriage, premature labor,
lbw, infant death
▫ Avoid raw/undercooked meats, fish, poultry;
unpasteurised milk, cheese, juices, raw sprouts
Nutrition in Pregnancy
• FETAL NUTRITION
▫ Fetal Growth: Impact of Maternal Malnutrition
 Vitamins and Minerals: inadequate nutrient storage
 Maternal folate, B6, and Fe requirements in
pregnancy increased by 50%
 Ca, PO4, and Vits A, D, E, K; requirements do not
increase above baseline
Nutrition in Pregnancy-Vitamins
• A and C – important elements in tissue growth
• B vitamins – co-enzyme factors in energy
production and protein metabolism
• Folate – to build red blood cells
• Vitamin D – absorption and utilisation of
calcium and phosphorous for fetal bone growth
Nutrition in Pregnancy - Folate
• Requirement: At least 600 mcg/day
• To build red blood cells, prevent neural tube defects.
Nutrition in Pregnancy - Calcium
No need for increased intake due to
increased absorption in the GIT and
increased bone resorption
BENEFITS TO FETUS
• Good supply essential for fetal
bone and teeth development
• Positive correlation with femur
length
BENEFITS TO MOTHER
• Reduces onset of hypertension,
pre-eclampsia and eclampsia
Nutrition in Pregnancy - Protein
Proteins are the growth element for body tissues and a
primary need during pregnancy. Needs are increased in
pregnancy to support:
1) Rapid growth of fetus
2) Development of placenta
3) Growth of maternal tissues
4) Amniotic fluid production
Protein Requirements - about 75g/d
▫ 925 g protein accretes in fetus and mother, rate of
accumulation highest in Trim 3
Nutrition in Pregnancy - Energy
requirements
Mother needs more calories to:
1. Support the increased metabolic load
2. Spare protein for added tissue-building
requirements
At least 36kcal/kg needed for efficient protein use
(nitrogen retention) during pregnancy
Nutrition in Pregnancy – Carbohydrate
Metabolism
▫ Glucose concentration increased by hormoneinduced insulin resistance
▫ Glucose is transferred to fetus down a
concentration gradient facilitated by glucose
transporters
▫ In late pregnancy when fetal demand high, mother
compensates by:
 Increased protein utilization
 Increased fat utilization
Nutrition in Pregnancy - Fat
Metabolism
▫ 25-30% energy from fat
▫ Necessary for supply of EFA, Fat Soluble Vitamins
 fetus and newborn have limited capacity to
synthesize omega 3 and 6 (DHA)
 Omega 3 and omega 6 used for membrane
synthesis: brain growth and development
Mental development
and function
Early
nutritional
exposure
Stature and mass
Body composition
Work capacity
CHO metabolism
Fat metabolism
Prot. metabolism
Obesity
Diabetes
Hypertension
Heart disease
Cancer
Nutrition in Pregnancy-Special Groups
Teenage mothers
• Increased nutrient intake for both mother’s growth and
fetus
• Increased risk of hypertensive disorders of pregnancy,
preterm, lbw babies
Older mothers (>35 years old)
▫ Pre-existing illnesses
▫ Increased risk of developing gestational DM, HTN
▫ Chromosomal abnormalities
▫ Multiple gestation with increased nutrient needs
Nutrition in Pregnancy-Diabetes Mellitus
• Preconception counselling aimed at achieving HbA1C
<7% to reduce the risk of congenital anomalies
• Women with pregestational diabetes should have a
baseline ophthalmology exam in the first trimester and
then be monitored every trimester
• Due to alterations in red blood cell turnover, the A1C
target in pregnancy is <6%
• GDM should be managed first with diet and exercise,
and medications should be added if needed.
Nutrition in Pregnancy - Collagen vascular
diseases
• SLE increases risk of spontaneous abortion, intrauterine
death, pre-eclampsia, IUGR and preterm birth. SSA and
SSB antibodies can lead to fetal heart block and neonatal
lupus.
• Prognosis for mother/child is best when disease is
quiescent for 6 months prior to pregnancy with normal
renal function
• Flares of SLE are uncommon during pregnancy and are
often easily treated with steroids.
• Monitor SLE disease activity with clinical history,
examination, and laboratory tests at least once per
trimester (strong suggestion)
Nutrition in Pregnancy
1. Importance of periconceptional nutrition
2. Impact of maternal nutrition on early fetal
development
3. Role of the placenta in fetal nutrition
4. Effect of pregnancy on nutritional
requirements
5. Dietary and weight gain recommendations
Dietary and weight gain recommendations
Energy Metabolism In Pregnancy
▫ Additional 300 Kcal/day average increased requirement
in Trim 2 & Trim 3
▫ Recommended Weight Gains
The Institute of Medicine’s pregnancy weight gain
recommendation guidelines for 2009 are as follows:
• Underweight - 28-40 lbs
• Normal weight - 25-35 lbs
• Overweight - 15-25 lbs
• Obese - 11-20 lbs
© 2 007 Thomson W a dsworth
Nutrition in Pregnancy- Key Concepts
Maternal diet and nutrient stores together provide for fetal
needs:
i. Folate and Fe needs increase dramatically (50%)
ii. Energy needs increase 10-15% in Trims 2 & 3
iii. Maternal Fe, B12 stores are important to cover some of
the increased requirements
iv. Fetal brain development impaired by inadequate energy,
protein, EFA and Fe
v. recommended weight gain dependent on pre-pregnancy
BMI
Nutrition in Pregnancy -Key Concepts
Most nutrient energy is transferred to the
fetus as glucose
i. glucose is the fetus’ main energy source
ii. Glucose is transferred down a
concentration gradient
iii. Maternal insulin resistance increases
plasma glucose
LACTATION
Objectives:
1. Identify benefits of breast feeding
2. Describe milk production regulation
3. Detail nutrient requirements during
lactation
4. Advise on dietary needs in lactation
LACTATION- Benefits of breastfeeding
▫
▫
▫
▫
▫
Provides optimal nutrition
Reduces incidence and
severity of infections
Protects against food
allergies, eczema
Increased cognitive, visual
development
Promotes bonding
LACTATION-Process
▫
Signaling- infant can signal to the mother by
vocalization, feeding demands, and nonnutritive suckling
▫ Positioning
▫ Latch-on
▫ Suckling
 Hormone release
 Letdown response
 Milk secretion into alveolus
 Milk ejection
 Milk extraction by infant
HORMONES OF LACTATION
1.
Prolactin
i. Prepares breast in pregnancy
ii. Suckling releases prolactin
iii. Initiates and maintains milk supply
2.
Oxytocin
i. Suckling releases oxytocin
ii. Contracts myoepithelial cells - ejection of milk from alveoli
into ducts
3.
Feedback Inhibitor of Lactation (FIL)
i. Whey protein found in breasts that enables the mammary
glands to regulate milk production.
ii. When a woman's breasts are full or engorged, they contain
more FIL than when they are empty.
Nutrient content of breast milk
These are relatively independent of maternal diet
(except for fluid intake)
1. Carbohydrate - lactose, oligosaccharides
2. Fat - triglycerides, fat soluble vitamins
3. Protein-casein 30%: whey 70% (lactoferrin,
lactalbumin, secretory IgA)
4. Minerals (Na, K, Cl, Ca, Mg)
5. Docosahexenoic acid (DHA) and arachidonic
acid (AA)
Nutrient content of breast milk
• Nutritional composition of breast
milk changes as the infant grows
• Colostrum is lower in fat, higher
in protein, vitamin A, minerals,
and antibodies
• Mature breast milk is high in
lactose, fat, B vitamins and lower
in fat-soluble vitamins, sodium,
and other minerals
• The American Academy of
Pediatrics recommends
supplementing breast-fed babies
with vitamin D drops
Colostrum
(day 1-7)
Transitional
(day 7-14)
Mature milk
(> day 14)
Nutrient content of breast milk
Cow’s milk is not recommended in children <
1 year
• Compared with cow’s milk, breast milk contains:
i. More carbohydrate
ii. Less protein
iii. Similar fat
iv. Oligosaccharides
v. Higher whey % (70%)
vi. Less Fe, Ca and PO4
•
LACTATION
• Some women may not be able to breast-feed, eg:
▫ AIDS,
▫ human T-cell leukemia,
▫ active tuberculosis,
▫ receiving chemotherapy and/or radiation,
▫ using illegal drugs
Infants with galactosemia cannot metabolize
lactose and should not be breast-fed
LACTATION -KEY CONCEPTS
1.
Advantages include infant nutrition, reduced infections
(GI, ENT), reduced food allergies, increased cognitive
and visual development
2.
Milk production not significantly affected by maternal
diet. Maternal requirements 500 Cal/day and fluids.
3.
Fatty acid composition of breast milk does reflect
maternal diet
4.
Breast milk is totally sufficient for first 4-6 months
(exceptions – Vits D (sunlight), K (inject at birth)
5.
Effective nursing requires proper position and effective
latch-on
GROWTH AND DEVELOPMENT: THE
TERM INFANT
▫
▫
▫
Infants grow rapidly - double weight in 6 months
Limited GI and renal capacities
 Cow’s milk and solids are less well tolerated
GI Tract Development
 Birth - swallowing reflexes immature
 Pancreatic amylase secretions begin at 6 months
 1 year - can chew solids & swallow
▫ Can digest solids
▫ Can tolerate cow’s milk
▫ Small intestine enzymes begin to work
GROWTH AND DEVELOPMENT: THE
TERM INFANT
Fluid Requirements/day
 Insensible losses: 20 ml/kg
 Urine: 60-75 ml/kg
 Stool: 5 ml/kg
 Growth: 1-3 ml/kg
Total: 86-103 ml/kg/d
GROWTH AND DEVELOPMENT: THE
TERM INFANT
Energy Requirements
 93-120 Kcal/kg/d (more than twice adult
requirements)
 Components:
1. Resting Metabolic Rate -supports breathing,
circulating blood, organ functions, and basic
neurological functions (largest component)
2. Growth
3. Physical activity
4. Thermic Effect of Food - the extra energy your
body requires during digestion
GROWTH AND DEVELOPMENT: THE
TERM INFANT
Protein digestion:
 Infant capacity to digest and utilise is
limited and increases over first year of life
with gut maturation
 Requirement for protein is 2g/kg/d (0.8
g/kg/d in adults)
GROWTH AND DEVELOPMENT: THE
TERM INFANT
Lipids

Major energy source (50% E in breast milk)

Sole source of essential fatty acids-Omega 3:
linoleic and DHA

Carrier for fat soluble vitamins
GROWTH AND DEVELOPMENT: THE
TERM INFANT
Vitamins and Minerals

B12 – the term infant has 1 yr store. Vegan mothers
need supplement

Folate – Term infant stores limited. Breast milk and
formula adequate supply

Vit D – sunlight for 2 hours per week to convert
precursor to vitamin D to the active form. Breastmilk
is inadequate as sole source.

Vit K – all newborns given supplemental injection
GROWTH AND DEVELOPMENT: THE
TERM INFANT
Vitamins and Minerals - Iron

Term infant has iron stores to last 6 months

Fe deficiency occurs when mother is anaemic: inability to
transfer adequate amounts in Trim 3

Breast milk adequate if infant starts out with adequate stores.
Iron fortified formula an option.

Supplemental iron required if mother anaemic and has not
transferred enough Fe to fetus
•
Symptoms of Fe Deficiency: irritability, anorexia, poor weight
gain, poor cognition
GROWTH AND DEVELOPMENT: THE
TERM INFANT
Conditionally essential amino acids - normally nonessential but must be supplied by the diet in special
circumstances when the need for it exceeds the body's
ability to produce it (eg. prematurity, illness, stress)
 Taurine
▫ Retinal function and development
▫ Neurotransmitter
▫ Bile acid conjugation
 Cysteine
▫ Precursor to the antioxidant glutathione
(oxidant protection)
 Tyrosine
▫ Breast milk
Infant Feeding
▫ Introduce foods one
at a time
▫ Now recommended
that no restrictions
on food to be
introduced eg
meat, “allergy”
causing foods
▫ Single foods best
initially
Foods to omit
▫ Sweets of any kind
▫ No canned vegetables
 High in sodium
▫ Honey
 Risk of botulism
▫ Foods that cause risk
for choking
Foods at 1 year
▫ Same foods as rest of
family
Courtesy of : UNICEF
GROWTH AND DEVELOPMENT: THE
TERM INFANT - Key Concepts
1. Human milk is the most appropriate food for the
newborn
2. Energy requirements: 83-129 Cal/kg/d
3. Fluid requirements: 86-103 ml/kg/d
4. Human milk meets energy and fluid requirements
5. At birth, low secretion of digestive enzymes make
digestion impossible for solids or cow’s milk
6. Low renal solute capacity precludes high protein
intake. Kidneys mature in 4-6 months.
Summary
• Nutritional needs increased in pregnancy
• Fetal nutrition important in determining later
life outcomes
• Needs in infancy supplied by breast milk up to 6
months
NUTRITION CONCEPTS AND APPLICATIONS IN MEDICINE
Nutrition during the life cycle: an
overview
Badaloo
NUTRITION
• Overall, nutrition is the integrated processes by
which the cells, organs and whole body acquire
energy and nutrients to maintain body structure
and perform required functions
• Modulated by Physical activity and environmental
stressors
NUTRITION
• Nutrition is the relationship between food
composition, dietary intake and function
– What you eat (diet)
– What you are (form)
– What you can do (function)
• Nutritional metabolism?
• Chemical processes and reactions by which energy
and nutrients from foods are utilised by the body
• Demand led process at different stages of the
lifecycle
Meeting the demand at each stage
Recommended Intake for healthy,
well-nourished population
• Published for energy and nutrients
• national and international reports available
Terminology
• RDA: Recommended daily allowance
• RNI: recommended nutrient intake
• Requirements etc
Human energy requirements
Report of a Joint FAO/WHO/UNU
Expert Consultation, 2004
DIETARY PROTEINS.1
The nutritional value of dietary proteins depends
primarily on the capacity to satisfy the needs
for:
total nitrogen
 indispensable (essential) amino acids
dispensable amino acids
To allow for growth and maintenance of body
proteins, as well as other nitrogenous
compounds
DIETARY PROTEINS.2
• All of the 20 amino acids found in proteins are
essential for metabolism
• However, they are classified based on body’s ability
to make amino acids
• ESSENTIAL: not made in the body
– lys, met, ise, leu, val, trp, phe, thr in adults
– Plus arg and his in children
• NON-ESSENTIAL: made in the body
• CONDITIONALLY ESSENTIAL – inadequate synthesis of
non-essential amino acids
DIETARY PROTEINS
If one amino acid is limiting for protein
synthesis, others are oxidized/catabolized
If dietary energy is low, protein may be used
as a source of energy
Protein quality is based on ability to provide
the essential amino acids
STAGES
- Pregnancy & lactation
- infancy
- childhood
- adolescence
- adulthood
PREGNANCY.1
Dietary intake during pregnancy should provide the
energy and nutrients that will ensure:
i.
Optimum weight gain during pregnancy
ii. full-term delivery of a healthy newborn baby of
adequate size (3.1 to 3.6 kg) and appropriate body
composition
• by a woman whose weight, body composition and
physical activity level are consistent with long-term
good health and well-being
PREGNANCY.2
• The energy cost of pregnancy is determined
by the energy needed for maternal
gestational weight gain
• Energy needed is associated with:
– protein and fat accretion in maternal, foetal and
placental tissue
– increase in energy expenditure associated with
basal metabolism and physical activity.
PREGNANCY.4
• Evidence that the most significant predictor of
low birth weight and IUGR is:
– not attaining adequate maternal weight
– especially in developing countries with:
• inadequate health care systems
• and high prevalence of impaired growth during their
childhood
Recommended weight gain during pregnancy
Underweight
BMI
<18.5
Weight gain, kg
12.7-18.2
Normal
18.5-24.9
11.4-15.9
Overweight
25.0-29.9
6.8-11.4
Obese
≥ 30
At least 6.8
Body composition
• Many levels
• But 2 compartments frequently measured
– Fat and lean tissue
• Insufficient dietary protein and
micronutrients limits protein and lean tissue
synthesis
– thin fat (not detected by BMI)
– stunting
Foetal growth longitudinal study
Villar et al Lancet 2014
• Eight cities in Brazil, Italy, Oman, USA, UK, China,
India, Kenya
• Foetal growth and newborn length are similar
across the diverse geographical setting
• When mothers nutritional and health needs are
met and environmental constraints on growth are
low
• Indicates that the potential to grow is similar,
regardless of race/ethnicity and place of birth
Developmental Origins of Health and
Disease (DOHAD)
Barker’s theory since 1980s
• Infants nutrition and growth are influenced from intrauterine
and early postnatal experiences
• Can be related to risk of developing chronic diseases later in
life
• Eg. mother’s nutritional status (underweight, overweight,
excess wt gain), inadequate pre- and post-natal nutrition &
rapid catch-up growth
• Hence healthy habits and the prevention of disease must
begin from in utero
Barker : foetal
origins hypothesis
DOHAD
Lower birth wt (including lower normal range),
together with infant rapid catch-up growth, is
associated with risk of childhood and adult obesity
Thin babies – low muscle mass- at risk of Insulin
resistance , DM and adiposity rebound at early age
• Optimal nutrition during the first 1000 days of life
(conception to age 2y) with normal growth rate :
– lowers morbidity and mortality
– reduces the risk of chronic disease, and fosters
better development overall.
• The first 2 years of life is said to be a plastic period
for catch-up growth
• If children are undernourished by second birthday,
they could suffer irreversible physical and cognitive
damage
• Concern about rapid wt gain leading to risk of
obesity
WHO and UNICEF recommend
• exclusive breastfeeding for the first six months of life
• Around the age of six months, an infant’s need for
energy and nutrients starts to exceed what is
provided by breast milk
– developmentally ready for other foods.
• So introduce nutritionally-adequate and safe
complementary (solid) foods at six months
– together with continued breastfeeding
• Suboptimal breast feeding results in more than
800,000 child deaths annually (Black, Lancet 2013)
LACTATION
• well-nourished women with adequate
gestational weight gain
– increase food intake by 2.1 MJ/day (505
kcal/day) for the first six months of lactation
• Undernourished women and those with
insufficient gestational weight gain
– add 2.8 MJ/day (675 kcal/day)
• Exclusive breast feeding is found in only
~38% of infants 0 to 6 months old
• In many countries, few children receive
nutritionally adequate and safe
complementary foods
HIV & Breastfeeding
• Since 2010, WHO has recommended that mothers
who are HIV-infected take ARVs
– and exclusively breastfeed their babies for six
months
• then introduce appropriate complementary foods and
continue breastfeeding up to child’s first birthday.
• only stop breastfeeding once a nutritionally adequate
and safe diet without breast milk can be provided.
Assessment of nutritional status
• Different indicators based on reference growth
standards eg:
– weight for length/height (children & adults)
– BMI (children & adults)
– Mid-upper arm circumference
• Other indicators in children:
–
–
–
–
–
head circumference
subscapular and tricep skinfold for age
motor development milestone
weight, length, head circumference velocities
biochemical
Most recent reference: WHO growth
charts 2006: MGRS
• Data from six countries ( Brazil, Ghana, India,
Norway, Oman, USA): healthy, well-nourished, breast fed
• Previous NHANES reference data based on US
population- not all breast fed
• Potential to grow is similar, regardless of their
race/ethnicity and place of birth, if they are
breastfed, living in a healthy environment, and have
adequate nutrition.
• Mean length from birth to 24 mo in the 6 countries
were identical
MGRS: multicentre growth reference study
WHO 2006
• Created reference lines on growth charts called zscore (or SD score) lines
• They represent how far a measurement is from the
median (average).
• Z-scores less than -2 SD and greater than +2 SD
define abnormal growth
WHO 2006
Weight-for-length/height:
• measure of wasting
• between -2 and -3 Z-scores represent moderate
malnutrition
• < 3 Z-scores represent severe undernutrition
Length/height-for-age
• Similar categories for stunting
• Terminology:
– now using Severe Acute Malnutrition (SAM) vs older
Protein Energy Malnutrition (PEM)
Interpret trends on growth charts
• The growth of an individual child plotted over
time is expected to track fairly close to the
same z-score between -2 and 2 z-scores of a
given indicator.
• Growth lines that cross z-score lines indicate
possible risk .
No risk
Risk
Oedema masks low weight
Sharp incline or decline requires attention
Crossed 2 z-score lines: now stunted
Good trend- wt gain
slowed down in relation
to ht
Overweight: >
2 Z-score
Height (cm)
PREVALENCE OF MALNUTRITION
• Malnutrition encompasses both
undernutrition and a growing problem of
overweight and obesity
LANCET Nutrition Series 2013
• In children younger 5 yr
– wasting in 52 m
– overweight and obesity in 43 m
– stunting in at least 165 m
STUNTING
• Low length/height for age
• Prevalent in LMIC
• Associated with:
– increased risk of obesity and CND
– impaired cognitive function
– and low productivity.
Revision version (2013)
now available (free online)
Support Support optimal growth & development
Encourage Encourage fitness
Ensure
Ensure adequate nutrient stores for growth
demands
Establish
Establish healthful eating habits and physical
activity that will lower risk of chronic disease
School-Age Child –
Goals of nutrition management
Adolescence
• next stage of increased rate of growth is adolescent
period
• Increased demand for energy and nutrients
• period of significant gain in height
• can be shorter than height potential if nutrition is
inadequate especially in protein and micronutrients
Undernutrition
Inhibit bone
development
Lower peak bone
mass and
Adolescence –
nutritional
requirements
Lower height
velocity – stunting
Delayed/halted
puberty
Adulthood
Consume healthy diet
Consume fruits and vegetables daily
Maintain normal weight and physical activity
Ageing and older people.1
Many factors affecting food intake
Physiological Changes affecting appetite
– hormonal changes affecting appetite eg:
• increasing satiating effect of cholecystokinin
contribute to anorexia
Gastrointestinal tract
–
–
–
–
–
changes in smell & taste- diminished
dental health affects chewing
drugs
peristaltic activity- reduced gastric emptying
achloryhydria- impaired vit B12 absorption
http://www.endotext.org/male/male11/male11.htm
Reproduzido de Endotext.com: Age-Related Changes in the Male Reproductive Axis
Chapter 11 - Shalender Bhasin and Karen Herbst
Ageing and older people.2
Body composition
• Decrease in lean body mass (LBM) and increase in
body fat- faster after 80y
– Sarcopenia (reduced muscle mass and function)
– Loss of mobility, increased frequency of falls
– exercise and diet can reduce rate of decline decline in LBM
• Reduced bone mass
– may lead to osteoporosis
– risk of fracture
– Pathological
• visual, joint, hand tremors, hearing
• task of food eating difficult
Ageing and older people.3
• Immune function
– dysregulation in immune system
• Cognitive function
– Dementia ( 1 in 20 over 65y, 1 in 5 over 80y)
• Obesity
– Associated with high incidence of diseases eg
hypertension, diabetes, atherosclerosis, arthritis
and disability
• Social problems with housebound
Ageing - prevent or prepare for:
•
•
•
•
•
High costs of healthcare
Longer in-hospital stay
Dependencies
Need for institutionalization
High prevalence of chronic diseases
Nutrition throughout the life cycle-maybe
intergenerational
Source: Prepared by Nina Seres for the ACC/SCN-appointed Commission on the Nutrition Challenges of the 21 st Century.
QUESTIONS
7/11/2019
Nutritional Screening
Nutritional Assessment
- Undernourished patient
• Rapidly identifies patient at high nutrition risk
Dr. Taylor-Bryan
2019
NUTRITIONAL SCREENING TOOLS
• SGA – Subjective Global Assessment
• MUST- Malnutrition Universal Screening Tool
SGA
• “Subjective Global Assessment is a simple bedside
method of assessing the risk of malnutrition and
identifying those who would benefit from nutritional
support.
• Its validity for this purpose has been demonstrated
in a variety of conditions including surgical patients,
those with cancer, on renal dialysis and in the ICU.”
Dr. Khursheed Jeejeebhoy
SGA
On the basis of the history and physical
examination, 2 clinicians classified patients as
either :• well nourished
• moderately malnourished
• severely malnourished
1
7/11/2019
SGA
SGA
History
Examination
1. Weight loss in previous 6 months (kg /
proportionate loss)
2. Dietary intake in relation to patient’s usual
pattern
3. Presence of significant GI symptoms
4. Patient’s functional capacity or energy level
5. Metabolic demands of the patient’s underlying
disease state
1.
2.
3.
4.
SGA
• Based on history and physical examination
patient's nutritional status – determined
Loss of subcutaneous fat
Muscle wasting – quadriceps and deltoids
Presence of edema – ankles, sacral area
Presence of ascites
MUST
• A 5-step screening tool to identify adults at risk
of malnutrition and those who are malnourished
• Well nourished, moderate or suspected
• Subjective
MUST
The 5 ‘MUST’ Steps
• Step 1 - measure height and weight to get a BMI
score using chart provided
• Step 2 - note percentage unplanned weight loss
and score using tables provided
• Step 3 - establish acute disease effect and score
• Step 4 - add scores from steps 1, 2 and 3
together to obtain overall risk of malnutrition
• Step 5 - use management guidelines and/or
local policy to develop care plan
2
7/11/2019
Nutritional Assessment
Nutritional Assessment - importance
advice
• Defines a patient’s nutritional status
• Intervention
aggressive strategies
• To define malnutrition clinically and monitor
changes in nutritional status
• ↓risks and burdens of those diseases that have
a nutritional component
• In-depth evaluation
Nutritional Assessment
UNDERNUTRITION
Nutritional Assessment
• Components
- Dietary
PRIMARY
SECONDARY
• inadequate
dietary
intake
• disease states affecting….
ingestion, absorption,
transport, metabolism,
utilization or excretion of
nutrients
Eg. enterocutaneous fistula
- Anthropometric
- Biochemical status
- Functional & clinical status
Objectives of this lecture
Assessment of nutritional status
• clinical indicators
Clinical Assessment
• laboratory indicators
• functional tests
- immune function
- physical, social & psychological performance
3
7/11/2019
Clinical assessment
HISTORY
EXAMINATION
symptoms
manifestations
reported by the
patient
physical signs observations made
by a qualified
examiner
Clinical assessment
• Signs and symptoms - often non-specific and
develop during the advanced stages of
nutritional depletion
• Lab methods - an adjunct to clinical assessment
to detect marginal nutrient deficiencies before a
clinical syndrome develops
Clinical Assessment - HISTORY
Nutrient intake
Children
•
•
•
•
•
•
•
Anorexia
Actual intake over past few days
Frequency of feeding
Usual diet before ill
Breastfeeding history
Age of introduction of solid foods
GIT malfunction affecting intake, digestion or
absorption
• Medications - laxatives or diuretics
Clinical Assessment - HISTORY
Family
• Teenage mom, highest level of education of
caregiver, employment status
• Actual income of caregiver
• Family structure & support
• Living conditions
Adults
4
7/11/2019
Clinical Assessment - HISTORY
•
•
•
•
•
•
•
•
•
•
Wt change
Appetite
Satiety level
Taste change / aversion
Nausea / vomiting
Bowel habits – diarrhea / constipation
Chewing / swallowing ability
Pain while eating
Drug / alcohol use
Food allergies / intolerance
Clinical Assessment - HISTORY
•
•
•
•
•
•
•
Chronic disease affecting utilization of nutrients
Sx resection or GIT disease
Diet hx – usual meal pattern
Dietary restriction
Level of exercise
Medications
Ability to prepare / secure food
Clinical Assessment EXAMINATION
•
•
•
•
•
•
•
•
•
Anthropometry
Affect
Wasting
Pitting edema
Anemia
Jowls
Hair changes
Skin – dermatitis, candidiasis
Hepatomegaly
Laboratory indicators
• Anthropometry - undernutrition or overnutrition
• Laboratory assessment - detects subclinical
deficiency states / micronutrient status
Laboratory indicators
Laboratory indicators
• Objective means of assessing nutritional status
independent of emotional & other subjective
factors
• Supplement other methods of nutritional
assessment – dietary, clinical and
anthropometric assessment
• Confirms clinical diagnosis
5
7/11/2019
Biochemical tests
Biochemical Assessment
NUTRIENT LEVELS
Each tests costs money……….
• collecting the blood or urine
• Confirm clinical diagnosis of a deficiency
disease – scurvy, beri-beri, rickets
• equipment and chemicals
• Hematological diagnosis – Fe, folate, B12 def
• skilled laboratory worker’s time
• reporting & interpreting the test
• Community nutrition surveys to detect subclinical
micronutrient deficiency – iodine, iron
NUTRIENT LEVELS
BODY COMPOSITION
• Demonstrate objectively the response to a
nutrition education programme – reduction of
plasma cholesterol or urinary sodium
• Total body potassium – estimates body cell
mass
• Diagnose nutritional supplement overdosing (vit
A, pyridoxine)
• Creatinine-ht index – lean body mass (24hr
urinary creatinine is compared with expected
value for person of same ht & sex)
6
7/11/2019
SERUM PROTEINS
MONITORING - N2 balance
Albumin **
t1/2 21d
• Monitoring nutritional management in ICU with
parenteral nutrition and/or tube feeding
Transferrin (iron)
t1/2 9d
• Checking validity of food intake measurement –
24H urinary N indicates protein intake in people
with stable dietary pattern
Prealbumin =
t1/2 2-3d
transthyretin (thyroxine
& retinol binding protein,)
Retinol binding protein –
bound to pre-albumin –
transports retinol
 levels
• poor clinical
outcomes,
• ↑length of stay
• ↑risk for
complications,
death
t1/2 12h
Risk factors for malnutrition
• Stress / hypermetabolism without adequate food
intake
• Weight loss > 10% of usual body weight
• BMI <22 kg/m3
• Albumin < 35 g/l
• NPO > 7d
• Absence of - ability to swallow / functional GIT ,
poor oral intake
• Medications – laxatives, diuretics
Functional tests
• Measures extent of functional consequences of
a specific nutrient deficiency and hence has a
greater biological significance
Functional tests
Functional tests
• Functional biochemical tests
• Functional physiological/behavioral tests
7
7/11/2019
Functional biochemical tests
Functional physiological tests
Muscle function
Example
• Measurement of changes in blood components
or enzyme activities that are dependent on a
given nutrient
• Changes in muscle function (muscle contractility,
relaxation rate, endurance) may precede body
composition changes
• Impairment in hand grip strength
• Eg - whole blood Hb for iron assessment
• In critically ill pt, changes in muscle function may
alter respiratory function & precipitate respiratory
failure
Functional physiological tests
Muscle function tests
• Skeletal muscle function tests - generally
measure the function of the adductor pollicis
muscle after electrical stimulation of the ulnar
nerve
• Hand grip strength - a test of skeletal muscle
function
Functional physiological tests
Functional physiological tests
Immune function as a functional index of nutritional
status
• Not specific enough to detect individual nutrient
deficiencies
• Affected by other factors – emotional stress,
surgery, anesthesia, major burns, neoplasia,
viral infections
Functional physiological tests
Developmental responses
Immunological tests
• Lymphocyte count – reduced in malnutrition
(confounders – stress, sepsis, infection,
neoplasia, steroids)
• IgA antibody levels in saliva
Assessment of cognitive function:• Infants –Bayley Scales of Infant Development
• Older school child –IQ test performance
• Elderly – Mini Mental State Examination as a
screening measure of cognitive impairment
• Quantification of C3 levels
8
7/11/2019
Functional physiological tests
• Not suitable for large scale nutrition surveys –
too invasive, elaborate equipment
• Results difficult to interpret b/c of lack of cut off
points
• Less responsive than biochemical tests to small
changes in nutrient status
Remember !!
 Nutrition screening & assessment are not static
processes
 Continually reassess patient status & revise the
nutrition care plan on an ongoing process as the
patient’s clinical status and medical status
changes
• Many other non-nutritional factors may influence
their performance reducing their specificity
 Serum proteins are neither specific, nor sensitive
indicators of nutrition status
 As negative acute-phase reactants (albumin,
transferrin, prealbumin, RBP) the concentrations
of these proteins are affected by the acute
phase response
9
Dr. Joanne Smith
Epidemiology Research Unit
Caribbean Institute for Health Research
University of the West Indies
Mona, Kingston


The Study of the measurement of the human
body in terms of the dimensions of bone,
muscle and adipose (fat) tissue.
Measurements include:
◦
◦
◦
◦
Weight
Height/Length
Circumferences
Bioelectrical impedance (BIA)


Measurement of the size and proportion of
the human body
Aids in determination of body composition
Technique

Standardized procedures

Practice
 Accuracy and reliability




BMI
Waist-To-Hip Ratio (WHR)
Mid-upper Arm Circumference
Waist-To-Height Ratio (WHTR)

After measuring weight (kg) and height (m) ,
we can calculate BMI by using the following
equation
Weight (kg) = BMI
Height (m2)

WHR is a better indicator of cardiovascular
risk than BMI.
Waist circumference (cm) = WHR
Hip circumference (cm)
Waist to Hip Ratio Chart
Male
Female
Health Risk
Based Solely on
WHR
0.95 or below
0.80 or below
Low Risk
0.96 to 1.0
0.81 to 0.85
Moderate Risk
1.0+
0.85+
High Risk

A proxy for abdominal fatness
◦ Strongly correlated to abdominal fat measured by
imaging techniques

Predictor of CVD and Diabetes
Waist circumference (inches) = WHtR
Height (inches)



Ideally patient should have on minimal
clothing
Where necessary, remove outer
jackets, shoes, hair ornaments,
pockets items, belts, etc.
Some underwear may alter
measurements considerably (eg:
girdles, pantihose/tights)


An assistant may be required
Ensure that equipment is calibrated
and standardized

Use only standardized techniques

Practice!
• Arms
relaxed
• Palms
facing
thighs
• Body erect
• Heels, head,
scapula and
buttocks
should* touch
board
Flat, level
surface
Height – position of feet





Barefoot
Heels together
Heels touching pole*
Feet spread at 60o
Weight evenly
distributed



Remove protruding
hair objects
Head erect
Eyes focused straight
ahead

Frankfurt plane

Check spirit level
Height
• Press beam firmly on
head
• Verify measurement by
pulling down beam twice
• Measure to nearest
0.1cm
• Record immediately




Calibrate scale daily
Clean scale before each
patient
Adjust scale to read
‘kg’
Turn on and ‘zero’
scale
• Light clothing
• Body erect
• Arms relaxed
• Palms facing thighs
• Weight evenly
distributed
Feet on centre of
scale, toes apart
Measure to 0.1kg

Waist

Hip

Mid upper arm

Participant in minimal clothing

Flexible, non-stretchable, fibreglass tape

Measure on right side of body




Hold ‘zero’ end of tape below measurement
value.
Tape should be snug, slightly compressed (not
tight)
Measure to nearest 0.1 cm
Repeat measurements for discrepancies of 0.5
cm or more between readings


Measurer faces subject
Natural waist narrowest part of
torso as seen from
front
or

Halfway between the
lowest rib and iliac
crest approximately

Minimal clothing

Measure to the right


Ensure tape is
horizontal & parallel to
ground
Verify by standing to
side and back of
participant




Take measurement at
end of normal
expiration
Arms to side
Measure to nearest
0.1cm
Record immediately


Abdominal obesity is classified as a waist
circumference of >102 cm for men and >88
cm for women.
Measurement of the waist circumference
contains information about the central
distribution of body fat.




Measure to the right
Pockets empty, minimal
clothing
Point of maximum
extension of buttocks
Ensure tape is horizontal
& parallel to ground

Arms to side

Measure to nearest 0.1cm

Record immediately
Acromion
process of
scapula
Arm bent 90o
Palm facing
upward
Olecranon
process of
ulna
Mid point*




Arms hanging freely
at sides
Palm facing thigh
Tape perpendicular
to long axis of arm
Tape should be snug
◦ Not tight nor loose

0.1cm
• Tape should be horizontal and parallel to floor









Remove shoes and socks/stockings
Clean the back of the right hand and top of the
right foot with alcohol
Allow to air dry
Cut electrodes in half lengthwise
Place electrodes on sites with tips pointing to
outside
Black leads -right foot
Red leads - right hand.
Standing with feet shoulder-width apart and arms
at 45° to their bodies.
Record resistance & reactance



Measure with minimal clothing
Assistant is needed (mother can help)
Appropriate technique is important
1. Measure length for children less than
24 months of age.
2. Measure infant without shoes and
wearing light underclothing or clean
diaper.
3. Remove hair accessories that interfere
with measurement
4. Lay child on his back in the center of
the measuring surface.
5. Assistant cups the ears to hold the infant’s
head so the infant is looking upward and the
crown of the head is against the headpiece.
6. Bring knees together, extend both legs
and bring movable foot piece to rest against
heels.
7. Read measurement to the nearest 0.1 cm.

Weight-for-age

Length/Height-for-age

Weight-for-Length/Height

◦ Below -2 : Underweight
◦ Below -3 : Severely underweight
◦ Below -2 : Stunted
◦ Below -3 : Severely stunted
◦ Below -2 : Wasted
◦ Below -3 : Severely wasted
http://www.who.int/childgrowth/training/mod
ule_c_interpreting_indicators.pdf



http://www.who.int/childgrowth/standards/h
eight_for_age/en/
Use the tables for z-scores (boys and girls) to
find the values
% Median
◦ Individuals weight x 100
Median weight

Weight

Height

Waist Circumference

Hip Circumference

Mid-Upper Arm Circumference

After measuring weight (kg) and height (m) ,
we can calculate BMI by using the following
equation
Weight (kg) = BMI
Height (m2)
27/9/2020
MAJOR LEARNING OUTCOMES
▪ To define nutrition
▪ To outline the cellular processes underlying
normal health
NUTRITION AND CANCER
Dr Kwesi Marshall
Caribbean Institute for Health
Research
MBBS
Human Nutrition
MDSC3103
WHY STUDY RELATIONSHIPS
BETWEEN NUTRITION AND
CANCER?
▪ To outline the major stages of cancer cell
development
▪ To define cancer
▪ To outline the major hallmarks of cancer
▪ To identify evidence-based putative cancermodulating nutritional factors
▪ To present WCRF recommendations for
reducing cancer risk
There is compelling and accumulating
evidence that a myriad of nutritional
factors can influence the risks of
developing cancer.
WHAT IS NUTRITION?
▪ A system of processes through which nutrients
and energy are derived from food and drink to
enable growth, maintenance, repair and
reproduction.
CELLULAR PROCESSES
1
27/9/2020
‘NORMAL’ CELLULAR PROCESSES
▪ Cell signalling
- Autocrine
- Paracrine
- Endocrine
CANCER
▪ Cell growth
▪ Cell division/proliferation
▪ Cell differentiation
▪ Cell death
WHAT IS CANCER?
▪ A disease characterized by abnormal
proliferation of cells.
CARCINOGENESIS
▪ Cancer cells are produced by a multi-stage
process referred to as carcinogenesis.
MAIN STAGES OF CARCINOGENESIS
▪ Initiation
- DNA damage and/or mutations
(mutagenesis) in a single somatic cell
▪ Promotion
- Genetic and/or epigenetic changes that
accumulate over time
▪ - Results in increased rates of cell division or
reduced rates of cell death
FACTORS THAT INFLUENCE
CARCINOGENESIS
▪ Factors that can trigger cancer development are
referred to as initiators.
▪ Factors that facilitate cancer development once
it has started are referred to as promoters.
▪ In addition, factors that might protect against
the development of cancer are referred to as
anti-promoters.
2
27/9/2020
WHAT DEFINES A CANCER CELL?
TWO HERITABLE PROPERTIES:
▪ Cell reproduction in defiance of the normal
restraints on cell growth and division
▪ Invasion and colonization of territories normally
reserved for other cells
CANCER HALLMARKS
STAGES OF CANCER DEVELOPMENT?
▪ Over an extended time period, the inappropriate
excessive multiplication of cells can lead to the
formation of a tumour (neoplasm).
▪ Cancer cells arising from these tumours can
migrate and spread throughout the body and
potentially cause death of the entire organism.
CANCER HALLMARK 1
▪ There are several ‘hallmarks’ of cancer.
▪ Genomic instability
CANCER HALLMARK 2
CANCER HALLMARK 3
▪ Sustained proliferative signalling
▪ Evasion of anti-growth signalling
3
27/9/2020
CANCER HALLMARK 4
CANCER HALLMARK 5
▪ Resistance to apoptosis
▪ Replicative immortality
CANCER HALLMARK 6
CANCER HALLMARK 7
▪ Dysregulated metabolism
▪ Tumour promoting inflammation
CANCER HALLMARK 8
CANCER HALLMARK 9
▪ Immune system evasion
▪ Angiogenesis
4
27/9/2020
CANCER HALLMARK 10
▪ Tumour invasion and metastasis
CANCER CLASSIFICATION
SCHEMES
CANCER CLASSIFICATION SCHEMES
CANCER CELL CLASSIFICATION
Cancers are commonly characterized on the
basis of:
▪ Tissue/cell types from which they develop
▪ Primary site of tumour development
▪
▪
▪
▪
▪
▪
Carcinomas
Gliomas
Leukaemias
Lymphomas
Melanomas
Sarcomas
▪ Benign or malignant
CANCER SITE CLASSIFICATION
▪
▪
▪
▪
▪
▪
▪
▪
▪
Bladder cancer
Breast cancer
Cervical cancer
Colorectal cancer
Kidney cancer
Oesophageal cancer
Prostate cancer
Liver cancer
Lung cancer
CAUSES OF CANCER
5
27/9/2020
MAJOR CLASSES OF CANCER CAUSES
Broadly divided into:
▪ Endogenous causes
▪ Exogenous causes
▪ Chance!
ENDOGENOUS CAUSES OF CANCER
▪ Inherited germline mutations
- Tumour suppressor gene mutations
- Oncogenes (Ras, ERBB2)
▪ Somatic gene mutations that occur during the
life-course
▪ Epigenetic modulation (persistent, heritable
changes in gene expression, by processes such
as DNA methylation, histone acetylation, micro
RNA etc.)
EXOGENOUS CAUSES
ENDOGENOUS CAUSES OF CANCER
▪ Oxidative stress
▪ Chemicals
▪ Inflammation
▪ Infectious agents
▪ Hormones
-
Oestrogen
Insulin-like growth factor
Leptin
-
Viruses
Bacteria
▪ Ionizing radiation
▪ Nutritional pro-carcinogens
FIG. 3. FOOD, NUTRITION, OBESITY,
PHYSICAL ACTIVITY, AND CELLULAR
PROCESSES LINKED TO CANCER
EVIDENCE OF ASSOCIATIONS
BETWEEN NUTRITIONAL
FACTORS AND CANCER
6
27/9/2020
PUTATIVE DIETARY AND LIFESTYLE
PRO-CARCINOGENS
▪ Trans fatty acids
▪ n-6 PUFAs
▪ Saturated fatty acids
▪ Diet-derived mutagens
- Aflatoxin B
PUTATIVE DIETARY ANTICARCINOGENS
▪
▪
▪
▪
▪
▪
▪
▪
Carotenoids (lycopene, lutein)
Retinoids
Vitamin C
Vitamin E
Phytoestrogens
Phytosterols
Organosulphur compounds
Isothiocyanates
▪ Alcohol
▪ Obesity
MORE PUTATIVE DIETARY AND
NUTRITIONAL ANTI-CARCINOGENS
▪ Selenium
▪ Zinc
▪ n-3 PUFA
▪ Folate
PROBLEMS INTERPRETING POSSIBLE
DIET-CANCER ASSOCIATIONS
▪ Methodological
- Dietary intake estimates are typically
inaccurate
▪ Causal
- Diversity of potentially important and often
correlated dietary factors
- Relatively small influence (effect size) of
each factor on disease risk
▪ Energy restriction
▪ Dietary fibre
PANEL RECOMMENDATIONS
WORLD CANCER RESEARCH
FUND (WCRF)
EXPERT PANEL
RECOMMENDATIONS
The WCRF Expert Panel has made ten
recommendations, loosely divided into:
▪ Seven General recommendations
▪ Three Special recommendations
7
27/9/2020
RECOMMENDATION 1
RECOMMENDATION 2
BE A HEALTHY WEIGHT
BE PHYSICALLY ACTIVE
▪ Keep your weight within the healthy range and
avoid weight gain in adult life.
▪ Be physically active as part of everyday life –
walk more and sit less.
RECOMMENDATION 3
RECOMMENDATION 4
EAT A DIET RICH IN WHOLEGRAINS,
VEGETABLES, FRUIT AND BEANS
LIMIT CONSUMPTION OF “FAST FOODS” AND
OTHER PROCESSED FOODS HIGH IN FAT,
STARCHES OR SUGARS
▪ Make wholegrains, vegetables, fruit, and pulses
(legumes) such as beans and lentils a major
part of your usual daily diet.
▪ Limiting these foods helps control calorie intake
and maintain a healthy weight.
RECOMMENDATION 5
RECOMMENDATION 6
LIMIT CONSUMPTION OF RED AND
PROCESSED MEAT
LIMIT CONSUMPTION OF SUGAR SWEETENED
DRINKS
▪ Eat no more than moderate amounts of red
meat, such as beef, pork and lamb. Eat little, if
any, processed meat.
▪ Drink mostly water and unsweetened drinks
8
27/9/2020
RECOMMENDATION 7
SPECIAL RECOMMENDATION 1
LIMIT ALCOHOL CONSUMPTION
DO NOT USE SUPPLEMENTS FOR CANCER
PREVENTION
▪ For cancer prevention, it’s best not to drink
alcohol
▪ Aim to meet nutritional needs through diet
alone.
SPECIAL RECOMMENDATION 2
SPECIAL RECOMMENDATION 3
FOR MOTHERS: BREASTFEED YOUR BABY, IF
YOU CAN
AFTER A CANCER DIAGNOSIS: FOLLOW THE
RECOMMENDATIONS, IF YOU CAN
▪ Breastfeeding is good for both mother and baby
▪ Check with your health professional what is
right for you
SUMMARY
▪ Genetic and epigenetic events that lead to
cancers are mediated through endogenous
biological processes, exogenous mutagens and
chance.
SUMMARY
▪ Nutritional factors might play important roles in
protecting against certain cancers.
▪ Nutritionally based cancer prevention
recommendations from the WCRF emphasize
increased fruit and vegetable consumption,
reduced alcohol consumption, and elevated
physical activity.
9
SPORTS AND EXERCISE
NUTRITION
Dr Kwesi Marshall
Caribbean Institute for Health Research
MBBS
Human Nutrition
MDSC3103
MAJOR LEARNING OUTCOMES
 To identify the major fuel sources utilized during
muscular contraction under aerobic and
anaerobic conditions
 To discuss the advantages and disadvantages
of the major energy-generating systems
 To identify the factors affecting fluid loss during
exercise
 To outline selected specialized nutritional
protocols
WHAT IS NUTRITION?
 A system of processes through which nutrients
and energy are derived from food and drink to
enable growth, maintenance, repair and
reproduction.
WHAT DO WE MEAN BY SPORTS AND
EXERCISE?
 Sports and exercise comprise a huge range of
activities that involve physical exertion and skill
and are characterized by being both planned
and purposeful. For example:
- Sprinting
- Cycling
- Football
- Netball
WHAT BENEFITS CAN BE OBTAINED
THROUGH SPORTS AND EXERCISE?
 Health (physiological and psychological)
 Longevity
 Physical fitness
 Recreation/Fun
 Extrinsic benefits (trophies, recognition,
physical appearance, financial rewards)
COMPONENTS OF PHYSICAL
CONDITIONING
Nutrition and exercise are inter-related factors
influencing functional capacity:
 Increments in muscular work performance
mediated through skeletal muscle contraction
can be manifested by increased:
- Power
- Strength
- Speed
- Endurance
- Skill
- Muscle mass
FURTHER PERFORMANCE BENEFITS OF
PHYSICAL CONDITIONING
Changes in:
 Respiratory capacity
 Cardiovascular capacity
 Joint flexibility
 Body composition
NUTRITIONAL REQUIREMENTS
TO SUPPORT
SPORTS AND EXERCISE
FACTORS DETERMINING NUTRITIONAL
REQUIREMENTS
 Type of exercise
 Intensity, duration, and frequency of exercise
 Individual characteristics
- Sex
- Age
- State of maturation
- Level of physical conditioning
 Environmental conditions (e.g., temperature,
humidity, altitude)
NUTRITIONAL REQUIREMENTS

Energy

Carbohydrates

Proteins

Fats

Fluids

Vitamins

Minerals (electrolytes)
ENERGY
ENERGY
 Physical activity will increase daily energy
expenditure.
 Hence, recreational and elite athletes need to
increase food consumption to meet their energy
needs, according to the level of their daily
energy expenditure.
 Energy intake might be augmented by the
consumption of the appropriate foods/fluids.
CARBOHYDRATES
CARBOHYDRATES
 Carbohydrates are the fuel of choice for most
activities in varying conditions.
 Endurance events (e.g., triathlons) or
consecutive periods of exertion (events in
competition) without sufficient rest can lead to
glycogen depletion.
 Glycogen depletion, in turn, can result in
hypoglycaemia and exhaustion, which will
severely compromise performance.
 Therefore, ensuring carbohydrate needs are
adequately met should be a priority.
CARBOHYDRATE REQUIREMENTS
 60-65% of total energy should come from
carbohydrates.
- Athletes in endurance events may need to
obtain a greater proportion (65-70%) of
energy from carbohydrate.
 The goal should be to maintain maximal muscle
glycogen stores.
- Preparation for an event of long duration (>
90 min) might utilize a carbohydrate
loading plan.
- During prolonged activity (> 45 min), a
sugar-containing sports drink might be
effective.
PROTEINS
PROTEIN REQUIREMENTS (I)
 Amino acids derived from protein may be
oxidized to provide energy following glycogen
depletion
→ Increased muscle protein breakdown.
 Protein needs can be calculated as a
percentage of total energy or on a per kilogram
body weight basis
- For sedentary individuals, RDAs are 12-15%
total energy intake or 0.8 g/kg body weight
PROTEIN REQUIREMENTS (II)
Are there grounds for increasing protein intake?
 To compensate for increased amino acid
oxidation due to prolonged exercise
 To repair exercise-induced muscle damage
 To facilitate exercise-stimulated muscle
hypertrophy
PROTEIN REQUIREMENTS (III)
 Endurance athletes
-To repair damaged muscle fibres
- Some evidence that endurance athletes
should consume approximately 1.2 – 1.4
g/kg body weight
 Strength athletes
- To maintain a positive nitrogen balance so
as to maximize the hypertrophic stimulus
induced by resistance exercise
- Up to 1.6 g/kg body weight/day
FATS
FAT REQUIREMENTS
 Generally, protein and carbohydrate needs
should be calculated prior to estimating fat
requirements.
 Total fat intake is likely to be higher in athletes
who consume higher quantities of food to
maintain muscle mass.
 In contrast, severe fat restriction (<15% of
energy intake) may compromise performance
by impairing intramuscular triglyceride storage.
CHANGING NUTRIENT REQUIREMENTS
DURING EXERCISE
MAJOR SUBSTRATE SOURCES FOR
SKELETAL MUSCLE CONTRACTION
 Muscle glycogen
 Plasma glucose (Derived from liver glycogen or
obtained from the diet)
 Free fatty acids (plasma derived)
 Plasma derived lipoproteins
 Intramuscular triacylglycerols (IMTGs)
 Amino Acids
TYPES OF EXERCISE
 Metabolically, exercise can be classified into
two categories:
- Aerobic
- Anaerobic
FACTORS LIMITING ANAEROBIC
ENERGY PRODUCTION
 Lactate accumulation lowers pH resulting in
enzyme inactivation and muscle fatigue.
 Glycogen stores (muscle and liver) are limited.
 Quantitatively, the energy yield from anaerobic
glucose metabolism (3 ATP/M) is much less
efficient than aerobic glucose metabolism (42
ATP/M).
 Glucose derived from muscle glycogen stores
cannot be transferred to other tissues.
ENERGY STORES
 Energy stores in muscle supply requirements
for both immediate and prolonged exertion.
 Muscle energy stores can be replaced or
supplemented during and following exercise by
stores from outside muscle.
EFFECTS OF EXERCISE DURATION AND
ON SUBSTRATE UTILIZATION
 The rates and types of substrates utilized for
fuelling muscle contractions during exercise and
sports performance are influenced by varying
exercise intensities and durations.
EXPLOSIVE, HIGH INTENSITY EXERCISE
 High-intensity, short duration activity (e.g.,
sprinting) requires energy that is mainly
generated from carbohydrate sources
metabolized under anaerobic conditions.
MODERATE INTENSITY EXERCISE
 Low- to moderate-intensity, prolonged exercise
(e.g., jogging)
- utilizes carbohydrate stores for energy
generation primarily via aerobic pathways.
- Generates ATP from fats exclusively via
aerobic metabolism
LOW-INTENSITY EXERCISE
 Highly prolonged exercise (e.g., marathon
running), in addition to ongoing fat and
carbohydrate oxidation, also increasingly
mobilizes and oxidizes amino acids from
muscle protein exclusively via aerobic
pathways.
ATP
 Immediate form of useable energy for muscle
contractions.
 Intra-muscular ATP stores (24 mmol/kg dry
mass) can provide energy for brief, intense,
explosive muscle contractions.
 However, stores are extremely limited
- After 1-3 s at maximum levels of exertion,
stores are depleted.
 Consequently, muscle ATP has to be resynthesized.
MAJOR ATP SYNTHESIZING SYSTEMS
 Creatine Phosphate – ATP (phosphagen)
system
 Anaerobic (lactic acid generating) metabolism
 Aerobic metabolism
CREATINE PHOSPHATE (CP)
 Provides energy for short bursts of intense
exercise (3-10 s for maximal contractions).
 As ATP is utilized to generate energy, creatine
kinase liberates high-energy phosphate from
CP, thus regenerating ATP.
 Provides further energy by replenishing ATP in
the absence of oxygen.
 Creatine phosphate stores are quantitatively
greater than ATP reserves, but are still limited.
MUSCLE GLYCOGEN

Glucose is released from glycogen via
glycogenolysis.

Liberated glucose is then metabolized via
either aerobic or anaerobic means.

However, glucose generated from muscle
glycogen stores is not released into the
bloodstream.
- Consequently, the anaerobic capacity of each
skeletal muscle fibre is largely determined by
its own intrinsic glycogen content
(approximately 1.5 – 2 min).
FATTY ACID UTILIZATION

The potential supply of free fatty acids
released into plasma from lipolysis of adipose
tissue (subcutaneous and visceral) is
exceptionally high.

Muscle tissue also contains intramuscular
triacylglycerols mobilizable to provide energy.

However, the rate of ATP generation via fat
oxidation is slower than the overall rate of ATP
generation via muscle glycogenolysis.
- Fats are never the sole supply of fuel for
muscle contractions.
FIGURE 1: ACUTE METABOLIC AND
CONTRACTILE RESPONSES TO EXERCISE
(FROM EIGEN AND ZIERATH, 2013)
TABLE 1. FUEL SOURCES FOR MUSCLE
CONTRACTION (70 kg / 28 kg muscle mass)
Fuel Source
Maximal rate of ATP
production (mmol/s)
Muscle ATP
Total ~P available
(mmol)
223
Creatine Phosphate
73.3
446
Muscle glycogen to
lactate
39.1
6,700
Muscle glycogen to
carbon dioxide
16.7
84,000
Liver glycogen to
carbon dioxide
6.2
19,000
Adipose tissue fatty
acids to carbon
dioxide
6.7
4,000,000
FIGURE 2: THE EFFECT OF RACE
DURATION ON RUNNING VELOCITY
IAAF Ratified Track and Field Outdoor World Record Times 2010 (Male)
11
Usain Bolt (100m; 9.58s)
10
Velocity (m/s)
9
8
7
Haile Gebrselassie
(42,228m
2:03.59)
6
5
1
10
100
Running Time (s)
1000
10000
FLUIDS
SPORTS, EXERCISE, AND FLUID
REPLACEMENT
 Adequate hydration is probably the most
neglected dietary essential when considering
exercise performance.
 Extra heat generated by muscular activity has
to be rapidly decreased mainly through
sweating and respiration.
 Water lost as sweat can be considerable during
prolonged exertion (up to 1-2 L/h).
HYDRATION FOR SPORTS AND
EXERCISE
 Participants in exercise and sport need to use
the appropriate hydration/re-hydration
strategies to restore fluid balance.
 During long, strenuous exercise (particularly in
hot climates), persons should replace water lost
at regular intervals, in amounts sufficient to
maintain pre-exercise weight.
 Electrolytes and glucose added to re-hydration
beverages might be more effective than water
alone.
SAMPLE HYDRATION GUIDELINES FOR
DISTANCE ATHLETES
1. Do not restrict fluids before event.
2. Drink at least 1-2 cups two hours before event.
3. Drink at least 1-2 cups fluid immediately before
event.
4. Weigh in before event.
5. Drink at least 0.5-1 cup every 15-20 min.
6. Weigh in after event.
7. Drink 1-2 cups after event.
8. Drink at least 1 cup with and between meals.
SPECIALIZED NUTRITIONAL
PROTOCOLS
CARBOHYDRATE/GLYCOGEN LOADING
 In the 1960’s, muscle biopsies of endurance
athletes indicated that depleted muscle
glycogen stores were associated with reduced
exercise duration.
 Glycogen-loading programs were developed,
incorporating both training and dietary
manipulation, in order to bolster muscle
glycogen, thus increasing energy-creating
capacity and thereby endurance.
TABLE 2. A SAMPLE GLYCOGENLOADING PROGRAM
Phase
Days
before
event
Daily
training
load
1
7
Heavy
2
6
3
1
Daily
CHO
intake
Normal
Gradually Gradually
decreases increases
None
High
Goal
Glycogen
depletion
Glycogen
repletion
Glycogen
supercompensation
ADVANTAGES AND DISADVANTAGES
OF GLYCOGEN LOADING
Advantages
 Can prolong endurance capacity (>1 h / event).
 Can enhance performance for athletes
competing in several events per day.
Disadvantages
 Can result in excessive (water) weight gain.
-Increased muscle tightness might
compromise mobility and flexibility.
CREATINE LOADING
 Fatigue sustained during short-duration, highintensity exercise is associated with insufficient
ATP regeneration.
 Creatine supplementation (creatine
monohydrate: 20 g/day for five-six days, 5g/day
thereafter) appears to enhance repeated, shortduration, high-intensity exercise performance
and muscle mass.
- Further increases in creatine loads do not
seem to have any potentiating effect on
either creatine uptake or performance.
 Prolonged creatine use does not appear to
increase fat oxidation or overall oxidative
capacity in endurance athletes.
GENERAL AND SPECIAL
RECOMMENDATIONS
GENERAL RECOMMENDATIONS
 Pre-exercise/competition
- Carbohydrate and fluid intake should be
emphasized
 During exercise/competition
- Continued carbohydrate and fluid
consumption may be required during
prolonged exertion
 Post-exercise/competition
- Carbohydrate consumption should begin as
soon as possible after physical exertion for
optimal glycogen replenishment. Re-hydration
should also be emphasized.
GROUPS UNDER PARTICULAR FOCUS
 Pregnant Women
- Exercise and nutrition need to be carefully
monitored
 Exercising lactating women
- Require more fluid and energy
 Vegetarians
- A wide variety of foods/food combinations
should be encouraged to meet demands
 Children and adolescents
- Require more iron, calcium and fluids
SPORTS AND EXERCISE
NUTRITION:
REVIEW
SUMMARY
 Metabolically, exercise can be divided into two
broad categories – aerobic and anaerobic –
characterized by distinctive patterns of fuel usage.
 Carbohydrate consumption is the principal
macronutrient consideration for fuelling most
activities.
 Adequate hydration should be emphasized before,
during, and after exercise.
 Glycogen loading and creatine loading are
nutritional strategies designed to augment
performance in endurance and explosive activities,
respectively.
1
This session covers the way in which human body composition is defined in
nutrition and how body composition affects energy expenditure.
We then look at the components which make up total daily energy expenditure
and factors which affect how much energy is used. The session finishes with
an overview of the concept of energy balance
2
The energy metabolism of a person is defined as the sum of all chemical
reactions in which energy is made available and consumed in or expended by
the body.
The aim of energy in nutrition terms is to attain and maintain balance of
systems in the body. In keeping with the first law of thermodynamics, it can be
interpreted that energy can neither be created nor destroyed. Instead it is
transferred from one form to another or from one place to another. E.g. dietary
food energy can be converted to energy for brain activity or as fuel for muscle
work and exercise.
3
The composition of the body can be described at several different levels
however, as it relates to nutrition and energy we are most interested in the
molecular level which comprises the amount of protein and fat in the body as
well as water and minerals. When we consider whole body measurements in
nutrition the tissue systems are measured to assess lean, fat and bone mass and
composition.
4
In order to study body composition , body weight may be subdivided into two
or more components. This slide shows four different body composition models
that are used depending on the objectives of the measurement and the
questions to be answered.
5
The two compartment model is useful as the metabolic rate of LBM is higher
than that of fat mass. This is one reason why body composition is important as
it influences how much energy a person uses each day.
Body composition is also important as it is related to risk of several chronic
diseases including cardiovascular disease and some cancers. Risk of disease
increases with excess fat. Fat distribution is also important as risk is usually
more strongly related to abdominal fat
The normal range of body fat is higher in women than in men: 20-25% for
women and 12-15% for men
6
This slide show the average percent body fat at birth, in 10 year old children
and in adults. Percent body fat increases with age, particularly in women. The
sex difference in % fat becomes more marked after puberty
7
Other influences on body composition include:
Aging – there can be a decline in LBM, primarily loss of muscle mass in older
persons. This can be reduced if physical activity is maintained
Nutrition – under or over nutrition leads to changes in fat mass and lean body
mass
Activity – particularly strength training can increase LBM if there is no
accompanying weight loss. During weight loss activity can help to reduce the
amount of lean tissue that is lost. This is important as LBM influences energy
expenditure. If LBM is lost then after weight loss energy expenditure will be
lower and it will be easier to regain weight
Hormones and certain disease states can also affect body composition
8
There are four main component of energy expenditure as listed on this slide.
Each will be described in the following slides
9
Each component contributes a different amount of energy to the total value.
(Growth energy is not represented in this slide)
There are known determinants that will have an influence on each component
which accounts for individual variations.
10
The basal metabolic rate or BMR is the energy required by the body at
complete rest. It is measured with the person lying down in a thermoneutral
environment so that no energy is needed to keep the person warm or cool, (e.g.
shivering will cause an increase in energy output).
BMR should be measured in the post prandial and post absorptive state so that
no energy is being used to digest and absorb nutrients. The best time to do this
after a 12 hour fast when the individual has just awakened. For logistical
reasons, this measurement is often done in the morning, a few hours after
waking (e.g. at a lab) but they remain awake and in a rested state. This
measurement is termed Resting Metabolic Rate (RMR).
A common method for measuring this is by indirect calorimetry using a
ventilated hood as shown in the picture.
11
An estimate of BMR can be calculated from a person’s weight. There are
separate equations for men and women and younger and older adults
12
Energy is also need to ingest and digest food and for the absorption and
transport of nutrients. This is called post prandial thermogenesis or the
thermic effect of food.
The amount of energy needed is greater for larger meals and also depends on
the composition of the meal. Post prandial thermogenesis is higher after meals
high in protein or alchohol than after meals high in fat. Protein plays an
important role in weight regulation through satiety related to dietary
thermogenesis.
TEE = total energy expenditure
13
The final component of total daily energy expenditure is physical activity. This
is the most variable component among adults as it depends on the type of
occupation and also on the types of leisure activities that an individual chooses
to engage in.
Occupations can be grouped into light, medium or heavy categories depending
on the amount of energy required
14
The energy costs of each activity that someone participates in over a day can
be used to estimate their overall physical activity level. This is their total daily
energy expenditure expressed as a multiple of the BMR and depends on the
amount of time spent sleeping, the types of occupational and other activities
and the time spent doing these.
It can be calculated by multiplying the amount of time (in hours or portion of
an hour) spent in each activity by its energy cost. These are then added
together and divided by 24 (hours in a day) to get the overall or average
physical activity level
15
This slide gives some examples of the energy or Metabolic equivalent cost of
activities. The energy cost is expressed as a multiple of the BMR or RMR.
That is, for someone at complete rest whose expenditure is equivalent to the
RMR the energy cost is 1. Any activity above that is expressed as how many
times the RMR it requires . This ranges from sedentary activities such as
sitting which requires only 1.4 times as much energy as the RMR to heavy
activities which can require 8 times the RMR
The website link which is listed at the bottom of the slide gives the energy cost
of many more activities. This is often referred to as MET values or PAL
values.
16
The physical activity level or PAL categorisation has been revised to include
both occupation and leisure activities to describe an individual’s lifestyle. Thus
someone who was in a sedentary activity could have a moderately active
lifestyle if their leisure time was very active. This new categorisation also
gives a range of values rather than a single value per category
17
In children part of the daily energy requirement includes the energy required
for growth. It has been estimated that to gain 1g in weight requires 5 kcal or 21
kJ (1kcal = 4.2 kJ)
The energy for growth is a large proportion of total energy requirement in
infancy but is small relative to total energy during the rest of childhood.
At 1 month of age energy for growth is 35% of the total daily requirement but
by 12 months is 3% of the daily requirement
18
This slide shows the decline in energy expenditure PER KG BODY WEIGHT
from infancy to adulthood, with decrease in both BMR (shown in green) and
the energy needed for growth.
19
How much energy a person needs depends on their size and body composition.
Total daily energy expenditure is higher in larger persons (BUT not
expenditure/kg body weight)
As we saw earlier lean body mass has a higher metabolic rate than fat , so
persons with higher percent body fat will have a lower energy expenditure
Lower energy expenditure in women compared to men is due to smaller body
size and higher body fat in women
20
Energy expenditure per kg body weight is higher in children than adults. This
is due to energy needed for growth and differences in body composition.
Energy expenditure may decline in older adults, due to loss in lean body mass
and also decrease in activity levels
21
Climate can influence energy expenditure if energy is needed to maintain
body temperature. However, this influence is limited by appropriate clothing
and heating/cooling of buildings
There are also genetic influences on metabolic rate and on body composition.
Thus individuals of the same age, sex, weight and body composition can have
different metabolic rates
22
Energy expenditure can also be increased in persons with fever or burns
Endocrine disorders such as Hypo and hyper thyroidism also affect energy
expenditure through their influence on metabolic rate.
Total daily energy expenditure may also be increased during pregnancy
although reduction in activity may also occur
Some drugs can also influence energy expenditure through their effects on
metabolic rate
23
Up to this point we have been focusing on energy expenditure. The concept of
energy balance relates energy expenditure or the total daily energy use to the
amount of energy consumed or energy intake. Generally speaking, if energy
intake is consistently (over time) greater than energy output then this person
would be in positive energy balance and weight gain will occur.
Similarly, if energy output (increased physical activity) is greater than energy
intake (via reduced caloric intake) then this would create a negative energy
balance and the person would lose weight. No difference in intake or output
would create weight stability.
24
An individual who is neither gaining or losing weight and is therefore weight
stable, is said to be in energy balance if the energy consumed is equal to the
energy used.
This balance is not achieved daily but usually over a period of about a week.
Balance is usually achieved by changes in intake as this is more variable than
expenditure
Any change in expenditure is primarily due to chages in the physical activity
energy component
25
If energy intakes exceeds output or expenditure than a person is described as
being in positive energy balance. If this occurs something has to be done with
the extra energy available and it is used to increase body stores – mainly by
gaining body fat.
Over time the individual will attain a higher body mass and associated with
this will have a higher energy expenditure
26
If intake does not increase further then energy balance may be achieved,
however this will be at higher weight. Repeated periods of positive energy
balance will lead to overweight and obesity
27
Obesity increases the risk of many chronic non-communicable diseases which
you will learn about in more detail later in this course
28
There can also be situations where energy intake is less than the total daily
energy used leading to negative energy balance. If this occurs then the
additional energy needed is obtained by using energy from body stores. This
leads to a decrease in body size and associated lower BMR and total energy
output.
Negative energy balance can also lead to a reduction in physical activity so as
to reduce overall energy expenditure
29
Reduction in body size and in physical activity will lead to a lower energy
expenditure. If intake remains unchanged it is possible that energy balance
may again be achieved. Repeated or prolonged negative energy balance leads
to undernutrition
30
In children negative energy balance can lead to reduced growth and
undernutrition. In early childhood this can lead to poor development because
of the impact of undernutrition on brain growth and development. The
reduction in physical activity can also affect development by limiting
children’s exploration of their environment
Adults who were undernourished as children or who are currently
undernourished may be less active and less able to do physical work
31
32
In summary we have seen that body composition affects risk of certain
diseases and also influences energy expenditure. Energy expenditure in
particular physical activity level can also have a direct affect on health.
In combination with energy intake, energy expenditure will determine energy
balance and the maintenance of optimal nutritional status or the development
of a nutritional state of excess energy leading to obesity or to undernutrition.
Both of these states influence health and risk of disease
33
Assessing Nutritional Status
Dr. Joanne A. Smith
Epidemiology Research Unit
Learning Objectives
By the end of this lecture the student should be able to:
• Define and explain the parameters that comprise nutritional status
• Explain different methods of assessing nutritional status
• Explain the use and applications of basic anthropometry and diet
in assessing nutritional status in population groups
Nutritional Status
• Nutritional status is the current status of a person or population group,
related to their state of nourishment (consumption and utilization of
nutrients).
• Optimal nutritional status is a modifiable and powerful element in
promoting health, preventing and treating diseases and improving the
quality of life.
Introduction
❖ The nutritional status of an individual is often the result of many
inter-related factors.
❖ It is influenced by food intake, quantity and quality, and physical
health.
❖ The spectrum of nutritional status spreads from obesity to severe
malnutrition
Healthy Nutritional Status
• When the dietary supply of energy and nutrients is sufficient to support
the physiological and metabolic needs of the individual
• Normal nutritional status results from supply being sufficient to
support the requirements, and therefore affects a patient’s response to
illness or injury
• Excesses or deficiencies of intake will lead to imbalance and if
prolonged can lead to poor nutritional status
Healthy Nutritional Status
• Important in high risk groups
•
•
•
•
•
Children
Pregnant women
Elderly
Immunocompromised patients
Injured
• Undergoing rapid changes in growth or development or abnormal
metabolic changes
Questions to ask
• Does supply meet demand?
• Is there balance?
• What are the signs of imbalance?
• Understand what is a ‘normal’ vs ‘abnormal’ state and whether these
changes are part of the acute phase or chronic phase of the disease
Changing Nutritional Status
• Nutritional balance occurs when the necessary dietary nutrients are
fully absorbed, utilized and stored in appropriate amounts.
• Nutritional Imbalance can occur with
• Intake vs Absorption: eating disorders, GI disturbances, surgery and
malabsorption states
• Utilization vs Losses: infection, trauma, burns, surgery, diarrhea and vomiting
• Nutrient Storage: obesity, diabetes, hypercholesterolaemia and fatty liver
Purpose
The purpose of nutritional assessment is to:
• Identify individuals or population groups at risk of becoming
malnourished
• Identify individuals or population groups who are malnourished
Purpose cont’d
• To develop health care programs that meet the community needs
which are defined by the assessment
• To measure the effectiveness of the nutritional programs and
interventions once initiated
Objectives
What do you look for when determining nutritional status?
• There are 3 basic objectives:
1. Dietary intake and pattern
2. Physical growth characteristics or changes in growth patterns
3. Signs of nutrient deficiency disease or illnesses associated with excess
Stages in the Development of a Nutritional Problem
Stage
Depletion Stage
Method Used
1
Inadequate Diet
Dietary
2
Level in reserve tissue stores
Lab
3
Body fluid stores
Lab
4
Tissue Function
Anthropometric/Lab
5
6
Nutrient dependent enzyme
activity
Functional change
7
Clinical Symptoms
Clinical
8
Anatomical Sign
Clinical
Lab
Behavioural/Physiological
Methods of Assessment
Nutrition is assessed by two types of methods: indirect and direct.
The indirect methods use community health indices that reflect
nutritional influences.
The direct methods deal with the individual and measure objective
criteria
Indirect Methods
These include four categories:
• Ecological variables including crop production
• Economic factors e.g. per capita income, household income,
population density, food availability and prices
• Cultural and social habits
• Vital health statistics particularly infants & under 5 mortality and
other health indicators
Direct Methods
These are summarized as ABCD
• Anthropometric methods
• Biochemical, laboratory methods
• Clinical methods
• Dietary evaluation methods
Objectives of the Nutritional Assessment
• To understand and interpret the role of these data obtained during
your assessments.
• These include:
•
•
•
•
•
Medical History
Anthropometry
Biochemical Investigation
Clinical/Physical investigation
Dietary Assessment
• Collected through the collaborative health team
Objectives of the Nutritional Assessment
• While used mainly for screening healthy patients it is also an
essential component of the nutritional care of hospitalized
patients, e.g.
• Pre-operative status (cancer, CVD, GI disease)
• Type of Surgery (GI tract, transplant surgery (kidney or heart)
• During recovery from surgery/acute illness/injury (fever, infection,
dehydration, diarrhea, nausea, oedema, weight change)
Medical History
Client History
• Medical history
• Presence of disease or risk factors
• Weight history
• Family and Social histories
• Medication or drug use
• Behaviour, client perceptions and beliefs
• Cultural indicators
Anthropometric Methods
• Anthropometry is the measurement of body height, weight and
proportions.
• It is an essential component of clinical examination of infants, children
and pregnant women.
• It is used to evaluate both under and over nutrition.
• The measured values reflect the current nutritional status and do not
differentiate between acute and chronic changes.
Anthropometry
• Stature
• Height/Length, Height-for-Age (Ht/Age)
• Weight/Weight change
• Weight-for-Age (Wt/Age), Body Mass Index (BMI)
• Circumferences
• Head, waist, hip, chest, mid-upper arm
• Body composition
• Skinfolds, bioelectrical impedance analysis (BIA), total body water, chemical
analysis
Cut-off/Reference Points
• Most features of nutritional status can be measured
• Reference points: are indicators used to determine the presence or
absence of a condition
• The values are not diagnostic but should be interpreted as ‘indicators
of risk’
Interpretation of cut-off/reference
There are 3 questions to consider:
• Is it clinically significant?
• Is the person healthy otherwise?
• Is it economically feasible to treat?
• Both treating the patient and the hospital costs associated with treatment
• Is it suitable for the individual?
• Race, sex, socioeconomic status (SES) and age
Nutritional Indices in Adults
• The international standard for assessing body size in adults is the body
mass index (BMI).
• BMI is computed using the following formula:
BMI = Weight (kg)/ Height (m²)
• Evidence shows that High BMI (obesity level) is associated with type 2
diabetes and high risk of cardiovascular morbidity and mortality
BMI (WHO - Classification)
▪ BMI < 18.5
= Under Weight
▪ BMI 18.5-24.5
= Healthy weight range (normal)
▪ BMI 25-30
= Overweight (grade 1 obesity)
▪ BMI >30-40
= Obese (grade 2 obesity)
▪ BMI >40
= Very obese
(morbid or grade 3 obesity)
Childhood Indicators
• These are used primarily in children under 5 years old where the rate
of growth is most rapid
• Weight-for-Height : Wasting (low) or
Overweight/Obese (high)
• Height-for-Age: Stunting (low)
• Head circumference: brain development
• Mid-upper arm circumference: Wasting/Malnutrition Screening
• Skinfold measures: Malnutrition screening
Malnutrition – The Wellcome Classification
• This is a reference tool used for assessing undernourished children
suffering from protein-energy malnutrition. It uses a combination of
anthropometry and clinical signs associated with oedema
Oedema
% Expected Weight Present
for Age
60-80%
Kwashiorkor
<60%
Marasmic-kwashiorkor
Absent
Underweight
Marasmus
Malnutrition – The Waterlow Classification
• This measures the presence/absence of stunting and/or wasting.
• Wasting is determined by measuring the % weight-for-height = ((body
weight of child)/ (weight of a normal child of the same height)) *100
• Stunting is determined by the % height-for-age = ((height of child) /
(height of a normal child of the same age)) * 100
Waterlow Classification
Weight-for-Height
(Wasting)
Height-for-Age
(Stunting)
>90
> 95
Mild
80-90
90-95
Moderate
70-80
85-90
<70
<85
Normal
Severe
Biochemical Assessment
• Laboratory or biochemical assessments may determine the amount of
nutrients and/or regulatory hormones or enzymes in the body
• Examples include:
•
•
•
•
Vitamin A – dark adaptation response
Haemoglobin – anaemia if low levels are present in the blood
Iodine – which is associated with goiter in adults and cretinism in children
Lipids – associated with serum cholesterol levels
Biochemical Assessment
• Hemoglobin estimation is the most important test and is a useful index
of the overall state of nutrition. Other than assessing the presence of
anaemia it also tells about protein & trace element nutrition.
• Stool examination for the presence of ova and/or intestinal parasites
• Urine dipstick and microscopy for albumin, sugar and blood
Specific Lab Tests
• Measurement of individual nutrient in body fluids (e.g. serum retinol,
serum iron, urinary iodine, vitamin D)
• Detection of abnormal amount of metabolites in the urine (e.g. glucose
or amino acids)
• Analysis of hair, nails and skin for micro-nutrients.
Advantages of Biochemical Method
• It is useful in detecting early changes in body metabolism and nutrition
before the appearance of overt clinical signs.
• It is precise, accurate and reproducible.
• Useful to validate data obtained from dietary methods e.g. comparing
salt intake with 24-hour urinary excretion.
Limitations of Biochemical Method
• Time consuming
• Expensive
• They cannot be applied on large scale
• Needs trained personnel & facilities
Clinical Assessment
• It is an essential feature of all nutritional surveys
• It is the simplest and most practical method of ascertaining the
nutritional status of a group of individuals
• It utilizes a number of physical signs, (specific and non specific), that
are known to be associated with malnutrition and deficiency of
vitamins & micronutrients.
Clinical Assessment…cont’d
• Good nutritional history should be obtained
• General clinical examination, with special attention to organs like hair,
angles of the mouth, gums, nails, skin, eyes, tongue, muscles, bones
and thyroid gland.
• Detection of relevant signs helps in establishing the nutritional
diagnosis
Clinical Assessment
• Advantages
• Fast and easy to perform
• Inexpensive
• Non-invasive
• Limitations
• Would not detect early cases
Clinical signs of nutritional deficiency
HAIR
Spare & thin
Protein, zinc, biotin
deficiency
Easy to pull out
Protein deficiency
Corkscrew
Coiled hair
Vit C & Vit A
deficiency
Clinical signs of nutritional deficiency
Thyroid gland
• in mountainous areas and far
from sea places Goitre is a
reliable sign of iodine deficiency.
Clinical signs of nutritional deficiency
Joints & bones:
• Help detect signs of vitamin D
deficiency (Rickets) & vitamin C
deficiency (Scurvy)
Clinical signs of nutritional deficiency
Oral Cavity Area Clinical Manifestations
Lips
Cheilosis, Angular Fissures
Nutrient Deficiencies
Niacin, B6, Riboflavin,
Iron
Gingiva
Spongy, Bleeding, Abnormal
redness
Vitamin C
Tongue
Glossitis (inflammation of the
Folate, Niacin, Iron, B6,
tomgue – red, raw, fissured),
Iron, Folate and
pale atrophic, smooth and slick Riboflavin
Dietary Assessment
• Identifies the 1st stage of nutritional deficiency
• 1o deficiency – low levels in diet
• 2o deficiency – interference with digestion
• Several methods
• Establish requirements/ deficiencies
• Energy needs based on RMR + physical activity
• Supplement/vitamins
• Special dietary considerations
Dietary Assessment
• Nutritional intake of humans is assessed by different methods. These
include:
•
•
•
•
•
•
24-hour dietary recall
Food frequency questionnaire (FFQ)
Dietary history
Food dairy technique
Observed food consumption
Weighed food record
24 Hour Dietary Recall
• A trained interviewer asks the subject to recall all food and drink
taken in the previous 24 hours.
• It is quick, easy, and depends on short-term memory, but may not be
truly representative of the person’s usual intake
• A single 24 hour recall cannot be done (usually 2 weekdays and a
weekend day)
Food Frequency Questionnaire
• In this method the subject is given a list of food items to indicate
his or her intake (frequency and quantity) per day, per week and
per month.
• Inexpensive, more representative of daily intake and relatively
easy to use.
• Can be used in large epidemiological studies to investigate the
correlation between nutrients and disease
Dietary History
• Subjects are asked open-ended questions regarding usual
(present or past) dietary intake
• The information should be collected by a trained interviewer.
• Details about usual intake, types, amount, frequency and timing
needs to be obtained.
• Cross-checking to verify data is important.
Food Dairy
• Food intake (types and amounts) should be recorded by the subject
at the time of consumption.
• The length of the collection period ranges between 1-7 days.
• Reliable but difficult to maintain.
Behaviour – Estimating Barriers and Facilitators
• Your own personal attitudes
• Awareness
• Triggers
• Non-receptive Treatment Environment
• Small – hospital gowns, BP cuffs, tape measures, scales etc.
• Office furniture (chairs with arms vs without arms)
• Accessibility (wheelchairs)
• Readiness of patient?
•
•
•
•
Why now?
What changes will you have to make?
What will change if you succeed at the goal?
What is the effect on others?
Diagnostic Plan - Hypercholesterolaemia
• Fasting lipid profile for the patient with family history of heart disease
• Assess dietary intake of fats/high fat foods, excess calories (what foods?)
• Anthropometry
• Body mass index (BMI), % Body Fat, Waist Circumference
• Classify the patient (obese, overweight)
• Clinical
• Blood pressure
Diagnostic Plan - Malnutrition
• Anthropometry
• Weight-for-age; Height-for-age; head and mid-upper arm circumferences
• Wasted, stunted, undernourished?
• Diet
• Intake (recent and typical)
• Compared with recommended intake
• Biochemical
• Blood, urine, nutrient deficiencies, infection
• Clinical
• Oedema, hair flag sign, sunken fontanelle
Nutrition in the Community
Shelly McFarlane Ph.D.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Outline for Lectures
• Definition of Community Nutrition
• Describe the role of nutrition in public health.
• Identify major concepts in
•
•
•
•
nutrition assessment
community needs assessment
designing interventions
marketing and evaluation of nutrition-related programs.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Outline for Lectures
• Describe cross-cultural communication, food habits, and their
potential effects on the nutritional status of a variety of ethnic and
religious groups
• Identify major factors, challenges, and trends that influence nutrition
status in developing countries.
• Recognize the challenges facing governments in providing quality
health care to all citizens.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Definitions
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Community Nutrition
• Community nutrition incorporates the study of nutrition and the
promotion of good health through food and nutrient intake in
populations
• The community rather than the individual is the focus of interest.
• The focus is on the promotion of good health and the primary
prevention of diet-related illness.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Community
• A community may be any group of individuals,
•
•
•
•
Population of a town or country,
Residents of an old people's home.
Residents in a hospital
Residents in a geographical neighbourhood
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Public Health Nutrition
• Public health nutrition is a general approach, which focuses on
the research of disease prevention and quality of life
• The focus of interest is research on dieting and food science
• Community health nutrition is about the development of health
programs that promote nutritional services
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Public Health Nutrition
• Focuses on the promotion of good health and the maintenance of well
being or wellness through nutrition and the prevention of nutrition
related disorders in the population
• Assessment of the extent of the problem
• Raises awareness of nutrition related health problems
• Provides the education to promote healthy practices
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Issues and concerns
• Risks of dietary inadequacies - under nutrition, stunting, wasting,
micronutrient deficiencies
• Food security -meeting the needs of vulnerable groups
• Declining breast-feeding practices
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Issues and concerns
• Co-existence of under and over – nutrition
• Burden of chronic non-communicable diseases increasing rapidly
• Links between diet and chronic diseases
• Inappropriate dietary practices / poor food choices
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Trends in Nutritional Status in Jamaica - Children
under 5 years
Wasting by Sex
Overweight by Sex
https://globalnutritionreport.org/resources/nutrition-profiles/latin-america-and-caribbean/caribbean/jamaica/#status-children-nutrition
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Trends (%) in Nutritional Status in Jamaica – Adults
Nutritional Status
JHLS-2000(CI)
15-74 yrs
JHLSII-2008(CI)
15-74 yrs
JHLSIII- 2017 ( 15+)
Underweight (<18.5kg/m2)
4.9(3.4-6.4)
4.7(3.9- 5.6)
6.4(5.4, 7.5)
Normal (18.5-24.99 kg/m2)
49.4(46.2-52.5)
43.6 (40.8- 46.3)
39.8 (37.5,42.2)
Overweight (25-29.99 kg/m)
26.1(23.5-28.7)
26.4 (24.5- 28.6)
53.8 (51.5,56.1)
Obese≥30 kg/m2***
19.7(17.4-22.0)
25.3 (22.8- 27.4)
28.6 ( 26.8,30.5)
Increased WC***
35.6 (32.8-38.5
45.2(43.3-47.1)
43.7 (42.2,45.2)
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Dietary guidelines
• Intended to promote nutrition education and dietary guidance with the
aim of helping the general public make healthy food choices
• Nutrient and energy requirements and recommendations form the basis
of dietary guidelines
• Food-based dietary guidelines convert scientific knowledge into practical
messages
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Dietary guidelines
• Some basic components
• Eat a nutritionally adequate diet composed of a variety of foods
• Eat less fat, particularly saturated fat
• Adjust energy balance for body weight control - less energy intake, more
exercise
• Eat more whole grain cereals, vegetables and fruits, that is, eat more
foods containing complex carbohydrates and fibre
• Reduce salt intake
• Drink alcohol in moderation, if you drink
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Dietary guidelines
• These are utilised to form the basis for country specific guidelines which
take into account the local context and cultural factors.
• They may be presented as statements and or in pictorial format.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Dietary Guidelines- Jamaica
Food-based dietary guidelines for Jamaica: Healthy eating - Active living
The FOOD Plate
• Eat a variety of foods from all the
food groups daily
• Eat a variety of fruits daily
• Eat a variety of vegetables daily 4.
Include peas, beans and nuts in your
daily meals
• Reduce intake of salty and processed
foods
• Reduce intake of fats and oils
• Reduce intake of sugary foods and
drinks
• Make physical activity a part of your
daily routine
http://www.fao.org/nutrition/education/food-dietary-guidelines/regions/countries
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Dietary Guidelines- St Lucia
Its all in the cooking pot!!!!
• Always try to eat ground provisions, peas
and beans in your meals every day.
• Eat more vegetables and fruits every day.
• Buy less fatty and greasy foods and when
you cook, use less fat and oils.
• Use less salt, salted foods, packaged
seasonings and salty snacks.
• Choose fewer beverages and foods
preserved or prepared with added sugar.
• If you drink alcohol, do so in moderation.
• Drink water several times a day.
• Make physical activity part of your daily
life.
http://www.fao.org/nutrition/education/food-dietary-guidelines/regions/countries
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Dietary Guidelines- Guyana
• Every day eat a mixture of foods from the
food groups shown in the ‘stew pot’.
• Grow, store and prepare foods in a clean
and safe way.
• Use less salt in your food.
• Eat foods that are low in fat.
• Use less fats and oils in preparing and
cooking food.
• Make physical activity and exercise a daily
habit.
The guide chosen by Guyana to represent its guidelines is • It is advisable not to drink alcohol, but for
a ‘stew pot’ filled with six food groups: staples, vegetables,
those who do, not more than one drink
fruits, legumes, food from animals and fats. Outside the
per day is recommended.
pot are images of people doing physical activity.
http://www.fao.org/nutrition/education/food-dietary-guidelines/regions/countries
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Dietary Guidelines- Belize
• Choose different types of foods from all the
food groups daily.
• Eat more of different types of local fruits daily.
• Eat more vegetables daily. Choose different
types.
• Choose to eat wholegrain and ground foods
more frequently.
• Limit your intake of fats, sugar and salt.
• Use natural seasonings in food preparation
and cooking.
• Practice good hygiene when buying, storing,
The food guide chosen is a basket filled with seven food preparing and cooking foods.
groups (staples, vegetables, fruits, legumes, foods from • Keep active. Make physical activity a part of
your daily routine.
animals, fats and oils, sugars and sweeteners) in the
recommended proportion for a healthy diet. Images of
people doing physical activity adorn the basket handle.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
http://www.fao.org/nutrition/education/food-dietary-guidelines/regions/countries
www.uwi.edu/caihr
Dietary Guidelines- Grenada
• Eat a variety of foods.
• Eat larger amounts of fruits and colourful
vegetables.
• Eat less fatty, oily, greasy and barbequed
foods.
• Consume less salt, salty foods, salty
seasonings and salty snacks.
• Choose to use less sweet foods and
drinks.
• Drink more water. It’s the healthier
choice.
The graphical representation of Grenada’s dietary
• Drink little or no alcohol.
guidelines is a nutmeg cut in half. Inside one of the halves
• Be more physically active every day. Get
of the nutmeg the recommended food groups are
moving!
represented. Images of physical activity surround the
nutmeg.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
http://www.fao.org/nutrition/education/food-dietary-guidelines/regions/countries
www.uwi.edu/caihr
Dietary Guidelines- Caribbean
• Vegetables: 3-5 servings per day
• Fruits: 2-4 servings per day
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Caribbean diets
• While these are characterized by diversity among and within countries
some general trends are observed:
• High consumption of starches and cereals but tendency towards more
refined ones
• Proteins mostly from meats, poultry, fish. In some countries legumes also
popular
• Some fruits and vegetables but generally lower than recommended
• High consumption of fats and oils, tendency towards fried foods
• High consumption of sugars
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Percentage of Jamaicans who usually consume recommended fruits serving per day*, by the category of sex and
age, JHLSIII 2018.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Percentage of Jamaicans who usually consume recommended vegetable per day*, by the category of sex† and
age, JHLSIII 2018.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Sex-specific and Total Prevalence (%) and Confidence Interval [CI] of the Physical Activity
Level of 15 Years and Older Jamaicans, JHLSII 2008
Gender
Male***
Physical Activity Level
Female***
Total***
High
5.2 [3.7, 7.3]
1.5 [0.9, 2.5]
3.3 [2.6, 4.3]
Moderate
27.2[22.9, 31.9]
24.0 [20.9, 27.4] 25.6[22.8, 28.5]
Low
67.6 [62.9, 72.0] 74.5 [71.3, 77.5] 71.1 [68.0, 74.0]
*p < 0.05; **p < 0.01; ***p < 0.001.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Frequency of Fruit and Vegetable Consumption of
Jamaicans Aged 15+ Years by the Category of Disease,
JHLSIII 2018
Obesity
Fruit Consumption
Optimal
Sub-optimal
Vegetable
Consumption
Optimal
Sub-optimal
Diabetes
Hypertension
High
Cholesterol
23.9
76.1
26.1
73.9
25.4
74.6
25.9
74.1
40.9
59.1
46.8
53.2
40.8
59.2
37.7
62.3
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Food Security
• Food Security exists “when all people, at all times, have physical and
economic access to sufficient, safe and nutritious food to meet their
dietary needs and food preferences for an active and healthy life”
• Household food security refers to the ability of the household to secure
either from its own production or through purchases, enough food to
ensure adequate dietary intake of all its members
• Availability of food however does not guarantee access e.g. Within a
community a number of households may be malnourished even where
food supplies are adequate.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Factors affecting availability at the household level
• Availability of food through markets and other channels.
• Ability of household to acquire food
• depends on
• income levels
• purchasing power
• Desire to buy certain foods (household behaviour)
• Mode of preparation (availability of nutrients)
• Distribution among household members
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Food Security in Jamaica
100
90
80
66.5
70
66.6
66.5
Percent
60
50
40
30
28.9
28.3
28.6
20
10
4.6
5.1
4.9
0
High or Marginal Food Security
Low Food Security
Male
THE UNIVERSITY OF THE WEST INDIES | CAIHR
Female
Very Low Food Security
Total
www.uwi.edu/caihr
Factors affecting availability at country level
• Country’s capacity to import food is a function of several factors such as:
• - export earnings
• - world food prices
• - debt servicing obligations
• Marketing of local production
• Infrastructure ( e.g. roads, irrigation)
• Production/Supply
• Climate change
Large disparities in availability exist among countries and even within
regions of some countries
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Groups at risk of food insecurity
• Marginal farmers
• Poor, urban and rural
• Unemployed
• Landless
• Female headed households (some countries)
• Large households
• Elderly, homeless (esp. developed countries)
• Refugees
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Dimensions of Food Security Problem
• How many people are food insecure?
• 795 million people are undernourished / have inadequate dietary energy supply
(780 million in developing countries) FAO State of Food Insecurity 2015
• Some progress seen in reducing the prevalence of undernourished /hungry
persons over the last 2 decades.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Impact of food insecurity
•
•
•
•
↓ adult work capacity
↓ school performance
Social impact
Depressed economic growth and national development
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Policies and programs
• Growth monitoring and promotion (GMP) - The regular measurement,
recording and interpretation of a child’s growth in order to counsel the
caregiver and follow-up results
• Important for identifying and monitoring individuals, groups or
communities who are nutritionally at risk.
• GMP enables early diagnosis of health problems that affect growth so that
timely interventions can be instituted.
• Allows for better targeting of interventions.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Policies and programs
Primary care services for malnourished children (Nutrition Clinics)
• refer severely malnourished children with clinical symptoms to hospitals
• provide counseling and dietary support for moderately malnourished
children
• provide counseling for overweight/obese individuals
• conduct food demonstrations for parents/caregivers of malnourished
children
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Policies and programs
• Programs to reduce the prevalence of anaemia
– iron supplementation
– food fortification
– diet modification
• Targeted feeding programs
– school feeding programs
– food supplementation given at Maternal and Child Health and special nutrition clinics
• Promotion of breast feeding
Baby Friendly Hospital Initiatives
media campaigns
primary care services
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Policies and programs
• Programmes to improve access to Food
• Food Stamp and Food Price Subsidy - intended to increase purchasing
power - price controls for specific foods and/or government subsidies for
specific foods - stamps that give discount to the holder on specified foods.
• Conditional cash transfer Monetary benefit linked to fulfilment of set
criteria e.g. Programme for Advancement through Health and Education
(PATH) in Jamaica
• preschool children must attend child health clinics for all scheduled immunization
• school-aged children must attend 85% of session to remain in programme
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Policies and programs
• Nutrition education – e.g promote increased consumption of fruits and
vegetables, decreased consumption of saturated fats
• Provide diet counseling for clients with chronic noncommunicable
diseases in health centers
• Provide diet counseling for persons with HIV/AIDS
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Policies and programs
• Multi-sectoral health promotion initiatives – e.g worksite wellness
programs, exercise programs in public and private sector
• Food safety laws - Legislation, regulation and standards to protect
consumers from unsafe , low quality and nonlabeled foods
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Food Laws
• Protect the health of consumers by ensuring that food offered is safe and
fit for human consumption
• Prevent consumers from being cheated - ensure descriptions, labels and
advertisements do not carry false claims
• Ensure fair competition among traders
• Facilitate consumers to make healthy food choices by providing
information about the nutritional content of food
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Nutrition in the Community Part II
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Topics
• Food and nutrition surveillance
• Community level markers of poor nutrition
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Food and nutrition surveillance
• Food and nutrition surveillance is the continuous monitoring, analysis and
interpretation of the food and nutrition situation within a country.
• It is used to predict changes and to contribute to the design,
implementation and evaluation of measures to combat undesirable
trends.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Food and nutrition surveillance
• It is dependent on reliable data, routinely collected from the various
sectors related to food, nutrition and health.
• The information must be relayed to the decision makers on a timely basis.
• Food and nutrition surveillance is only successful if the information
collected is translated into action
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Purpose of Food & Nutrition Surveillance
• Monitor health and nutritional status of the population
• Supply reliable and sustainable data on the nutritional status of people at
the national and international levels
• Show trends and enable local comparisons
• Raise awareness about nutritional problems
• Provide guidance to health-related local intervention programs
Nutrition data is a vital indicator for the overall health and welfare of
populations especially where regular demographic and health surveys are
lacking.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Objectives of Food and Nutrition Surveillance
• To prevent short term critical reduction in food consumption.
• Programme management
• To collect data on nutrition programs which will give direction on their progress
and effectiveness so that decisions can be made to modify extend or terminate
them
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Objectives of Surveillance
• To provide information on which to base planning decisions
• – whether to initiate new measures to improve nutrition and for whom
• – how to target programs to have the desired effect
• – whether to modify current or planned policies and programs in light of the
existing nutrition situation, the changes causes.
• To assess and or monitor indicators related to nutrition as a basis for
directing funds towards particular nutritional problems
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Types of Food and nutrition surveillance
• Determining prevalence of malnutrition in young children and changes
over time
• Determining food consumption patterns, identifying undesirable trends
e.g. increases in consumption of fats
• Identification of groups at risk of nutrition related diseases
characteristics - age, gender, location, socio-economic status
• Determining the prevalence of nutrition related disorders and risk factors
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Surveillance Cycle
Data/Observation
Detect New
Problems
Monitor and
Evaluate
THE UNIVERSITY OF THE WEST INDIES | CAIHR
Decide on
Action/Intervention
Take Action
/Implement
www.uwi.edu/caihr
Principal Users of Surveillance Data
• Communities involved in the design, planning and management of
nutrition related programs
• Government authorities and Non-Governmental Organizations supporting
food security, health and nutrition related programs
• Food Aid agencies e.g. World Food Programme ( WFP)
• Donors
• Industries addressing nutrition and health related issues
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Community level markers of adequate or poor
nutrition
• prevalence of wasting and stunting in children under five
• height of children on entry to primary school
• prevalence of exclusive breast feeding - initiation, at 6 weeks, 3 months
• prevalence of overweight and obesity in different age groups
• food availability
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Sources of data
• Repeated nutrition surveys
• Community-based sentinel sites
• Data from mass screenings
• Data from feeding program admissions
• Data reported from health clinics
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Nutrition Education
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Dr. Joanne A. Smith
Epidemiology Research Unit
Caribbean Institute for Health Research
The University of the West Indies
Why?
 Surveillance/Screening
 Identify ‘at risk’ groups or individuals
 Inform policy
 Clinical
 ID & confirmation of nutrition related problem
 Screening for nutritional management
 Monitor changes in nutrition intervention
 Research
Who needs assessment?
Everyone!!
 Healthy individuals
 Monitoring
 All ages – infancy thru to elderly
 Particularly ‘at risk’ groups
 Hospitalized patients
 1o or 2o nutritional problems

Pre- or post surgery, fever, infection, dehydration, nausea, oedema, weight change,
impaired absorption, anorexia nervosa and malabsorption
Applications of Anthropometry
 Identify a person’s health risk and ideal state
 Total body fat vs intra-abdominal fat
 Monitor changes in body composition
 With disease (e.g. malnutrition)
 Growth (e.g. in children)
 Development (e.g. cognition)
 Age and maturation
 Assess effectiveness of nutrition/exercise interventions
 Formulate recommendations and prescriptions
 For both diet and exercise
 Formula feeding (TPN, infant)
Other Uses
 Ergonomics
 Making use of office furniture
 Investigations – I.D. Repeat offenders, impersonators
 Eugenics in Germany WWII (Differentiate between Jews vs Aryans
for ‘craniometric certification’)
 Biometrics
Which method to use?
 Health Status
 Age
 Patient compliance
 Number of Participants
 Time available for assessment
 Precision and accuracy required
 Single or multiple occasions (to assess changes in body composition
parameters)
Variability to expect
 Related to short term variations in body proportions
 Loss of stature and increase in abdominal and calf circumferences
with prolonged standing

1-2 cm in a day
 Day-to-day or monthly variability of weight



Intake and elimination of food and water
Menstruation/fluid retention
1kg/day and up to 3 kg+
 Other factors
 Patient compliance, ability to position correctly
Interpretation
 Time of measurement is therefore important
 Equations/reference data
 Appropriateness of method to objective
 Precision and accuracy of measurement
Stature
 Length – Age 2 and under (infant)
 Height – Age 2 years and older
 Usefulness
 Height-for-Age – Stunting
 BMI in association with weight
Body Weight
 Used to assess overall size
 Often used with measurements of stature
 Useful indicator of change during interventions
Circumferences
 Measures girth
 Head
 Children – brain growth, malnutrition
 MUAC (mid-upper arm circumference)
 Children (malnutrition), blood pressure cuff size, wasting, changes
in adults
 Waist and Hip
 Adults - obesity
 Chest
 Lung capacity
Diet
 Essential component in nutritional assessments
 Measures food consumption
 Individual, groups, household and populations
 Helps in understanding the diet-health relationship via nutrient intake
 Identifies 1st stage of nutritional deficiency
 Forms the base for nutrition education
Diet
 Total energy & macronutrients
 Vitamins/minerals, Food supplements
 Alcohol and Caffeine
 Meal pattern (type, frequency)
 Food/diet practices (religious, low salt, weight loss, insulin-meal timing)
Estimation of Caloric Intake
 Total daily caloric intake
 Caloric content of individual foods/meals
 Reference data
 Portion sizes – use standardized units only



Food models (generic, individual)
Utensils
Pictures
Energy Balance
 Macronutrients
 Carbohydrates
 Fat
 Protein
 > Weight Gain
 < Weight Loss
Energy value of foods
 Indirect/direct calculation
 Energy conversion factors are used
 To correct for energy losses

Digestion, absorption, incomplete oxidation
Available or metabolizable
energy content of food
Energy Value
1 kilocalorie = amount of heat/energy required to raise 1 kg H2O by 1o
1 kcal = 4.184kJ (kilojoules)
 Produced when food is oxidized
 Atwater / ‘fuel’ factors
 Kcal produced by 1g of a nutrient when oxidized
 Used in computing diets, energy value of foods
Atwater Factors
Nutrient
Carbohydrate
Protein
Long-chain Trigylceride
Medium-chain Trigylceride
Alcohol (spec. gravity ~0.8)
Intralipid 10% (spec. gravity 0.91)
Caloric content/g
4 Kcal
4 Kcal
9 Kcal
8.3 Kcal
7 Kcal
1.1 kcal/ml
Specific gravity x proof of alcohol x Vol (dL) = Alcohol (g)
2
Alcohol (g) x 7 = kcal Alcohol
Beverage
Unit
Alcohol
Kcal/Unit
86 proof liquor
2 oz
21 g
147 kcal
4% beer
12 fl oz
13.5 g
150 kcal
14.5% wine
3.5 fl oz
11.6 g
80 kcal
Examples
1 slice bread = 2g Pro + 1g Fat + 13g CHO = ~ 70 kcal
x4
x9
x4
Approximate caloric content
Food
Amount
kcal
Diet Soda (Diet Pepsi)
16 fl oz
0-2
Regular Soda (Pepsi)
16 fl oz
275
Jerk Chicken Breast (1)
3 oz
140
KFC Crispy Chicken Breast (1)
3 oz
490
Patty (veg/chicken/beef)
1
400-600
BK Whopper w/cheese & regular fries
1 each
950
Dietary Assessment
 Nutritional intake of humans is assessed by different methods. These
include:
 Food consumption data
 Observed food consumption
 Weighed food record
 24 hour dietary recall
 Food frequency questionnaire
 Dietary history
 Food dairy technique
Which method to use?
 Depends on the nature of the presenting nutritional disorder
 Short-term influence?

Allergies, diarrhea, vomiting
 Medium to Long-term influence?

Malnutrition, obesity, hypertension
Dietary Information required?
 Actual intake
 Short term
 Usual intake of a group or individual
 Medium to long term
 Pattern of food use (individual or group)
 Identifies habits, practices, attitudes
Who?
 Subjects – is the method appropriate?
 Age, education, nutritional status, motivation
 Personnel requirements?
 Trained nutrition professionals required?
 Personnel easily trained?
 Time requirements?
Feasibility
 Respondent burden?
 Time
 Motivation
 Social barriers
 Available resources
 Cost
 Ease of administration
 Availability/cost of equipment
 Lab requirements?
Macronutrients vs Micronutrients
 Most methods are limited to macronutrient determination (CHO, PRO
and FAT)
 Differences in nutrients actually absorbed
 Micronutrient composition
 Present in very small quantities
 Larger fluctuations

Food preparation, natural variability
Weighed Food Record
 Considered gold standard
 Weigh food before consumption and after , may need to
provide a duplicate
 Imposes considerable burden on participants
 Only relatively educated and literate persons can be used
 Participants may change eating habits
Dietary History
Subjects are asked open-ended questions regarding usual
(present or past) dietary intake
The information should be collected by a trained interviewer.
Details about usual intake, types, amount, frequency and
timing needs to be obtained.
Cross-checking to verify data is important.
Food Dairy
Food intake (types and amounts) should be recorded by the
subject at the time of consumption.
The length of the collection period ranges between 1-7 days.
Reliable but difficult to maintain.
24 Hour Dietary Recall
A trained interviewer asks the subject to recall all food and
drink taken in the previous 24 hours.
It is quick, easy, and depends on short-term memory, but
may not be truly representative of the person’s usual intake
A single 24 hour recall cannot be done (usually 2 weekdays
and a weekend day)
Food Frequency Questionnaire
In this method the subject is given a list of food items to indicate his
or her intake (frequency and quantity) per day, per week and per
month.
Inexpensive, more representative of daily intake and relatively easy to
use.
Can be used in large epidemiological studies to investigate the
correlation between nutrients and disease
Food Frequency Questionnaire
Limitations:
 Long questionnaire
 Errors with estimating serving size
 Needs updating with new commercial food products to keep
pace with changing dietary habits.
Interpretation of Dietary Data
1. Qualitative Method

using the food pyramid and the basic food groups method.

Different nutrients are classified into groups (fat and oils,
bread and cereals, milk products, meat-fish-poultry,
vegetables & fruits)

determine the number of servings from each group and
compare it with minimum requirement.
Interpretation of Dietary Data
2. Quantitative Method

The amount of energy and specific nutrients in each food
consumed can be calculated using food composition tables
and then compared with the recommended daily intake.

Evaluation by this method is expensive and time consuming,
unless computing facilities are available.
Nutrient Analysis
 Computerized nutrient databases
 Nutritionist 5 or Nutritionist Pro
 Diet Programs
 Food composition tables
 CFNI Food Composition Tables for the English-speaking Caribbean
 USDA Food Composition Tables
 Food Labels
 Direct Calorimetry of food samples
Questions????
Overnutrition I
Physiology of weight regulation
Michael Boyne
Tropical Medicine Research Institute
University of the West Indies, Mona
“Angie”
Angie is a 32 year old woman who has been struggling with her weight
for many years. She was overweight as a child, but this worsened
during her adolescence. She says that she “eats like a bird” and she
is confused how she could have gained so much weight. She thinks
there is something wrong with her metabolism. She takes several
medications for hypertension, hyperlipidaemia, and osteoarthritis (i.e.
amlodipine, lisinopril, atorvastatin and ibuprofen), and she also has
obstructive sleep apnea.
She lives with an overweight consort and they have been trying
unsuccessfully for 5 yrs to have a child. Her fertility evaluation is said to
be normal although she has irregular menses. She is convinced that
she needs to lose weight at all costs to improve her health and her
chances of becoming a mother. She works as a telephone operator,
has a long commute to work from Portmore, rarely exercises because
of her arthritis and she "does not like gyms." She buys her lunch at
work and there is no evening meal-planning by her consort who does
the majority of cooking.
Her weight is at least 160 kg which is the maximum weight recorded by
the scale. Her height is 157 cm and her waist circumference is 140 cm.
Apart from a very obese abdomen, her physical examination is
unremarkable
Is Angie obese? How do you know if
she is obese?
Obesity is just like
pornography
It’s “hard to define but I
know it when I see it”
Justice Potter Stewart, 1964
Jean-AugusteDominique Ingres
1780-1867
The Turkish Bath
1862
Harmensz
Rembrandt van
Rijn
1606-1669
Bathsheba
1654
Antonio Allegri, known
as Correggio
1489?-1534
Venus, Satyr and Cupid
Classification of obesity:
Body mass index
Grade
3
Degree of
Obesity
Morbid obesity
BMI
> 40
2
Obesity
30-40
1
Overweight
25-29.9
0
Normal weight
18.5-24.9
Children > 95th centile for BMI
Natural Progression of Weight Gain
Fat content: women> men
Gradual increase from pre-puberty to 60s then age-related loss
Eckel R H et al. JCEM 2011;96:1654-1663
Global Prevalence Rates of
Undernourishment and Obesity
Source: FAO for prevalence of undernourishment. Population Health Metrics 10 (22): 1-16 (2012).
Global Burden of Obesity in 2005
and Projections to 2030
Int J Obes 32: 1431-37 (2008).
Age-adjusted prevalence of obesity
in the African diaspora
Men
Women
40
30
20
USA
UK
Barbados
Jamaica
St. Lucia
0
Cameroon
10
Nigeria
Prevalence (%)
50
Obes Rev 1995; 3: 95-105S
Worsening adiposity in Jamaicans
Luke 2001
+ 7 kg increase in men
+ 14 kg in women
Weight change in the African Diaspora
Weight change (kg/yr)
Nigeria
3
2.5
2
1.5
1
0.5
0
-0.5
-1
Jamaica
USA
2.4
1.2
1.16
0.43
1.19
0.25
0.19
-0.05
<25
25-29
30+
-0.77
2
BMI category (kg/m )
BMC Public Health. 2008;8(1):133.
Obesity epidemic strikes U.S. pets
CNN February 4, 2012
• 41 million dogs and 47 million
cats are overweight or obese
• 53% of adult dogs and 55% of
cats were overweight or obese
• 25% of cats and 21% of dogs are
obese
• HTN, arthritis, T2DM, cancers,
life span shortened by 2-2.5
years
What are the health consequences of
overweight?
Prevalence of hypertension and
mean BMI in African diaspora
% Hypertension
35
Maywood
30
25
St. Lucia
Jamaica
20
15
Barbados
Cameroon urban
Cameroon rural
Nigeria
10
22
24
26
28
Body mass index
Am J Public Health 1997;87:160-8
30
32
Complications of Obesity
↑ Mortality
Pulmonary disease 1-14 years lost
abnormal function
obstructive sleep apnea
hypoventilation syndrome
Nonalcoholic fatty liver
disease
steatosis
steatohepatitis
cirrhosis
Gall bladder disease
Gynecologic abnormalities
abnormal menses
SCFE
infertility
polycystic ovarian syndrome
Osteoarthritis
Skin
Gout
Idiopathic intracranial hypertension
Stroke
Cataracts
Coronary heart disease
Diabetes
Dyslipidemia
Hypertension
Severe pancreatitis
Cancer
breast, uterus, cervix
colon, esophagus, pancreas
kidney, prostate
Phlebitis
venous stasis
Y-Y Paradox:
Limitations of BMI across populations
Yajnik CS and Yudkin JS. Lancet 2004: 363: 163
20
Brown/beige fat
Visceral Fat Distribution:
Normal vs Type 2 Diabetes
Normal
Type 2 Diabetes
Insulin Resistance:
Causes and Associated Conditions
Aging
Obesity and
inactivity
Medications
Rare
disorders
Genetics
INSULIN
RESISTANCE
Type 2
diabetes
Hypertension
PCOS
Atherosclerosis
Dyslipidemia
23
Obesity and Metabolic Risk •
Abdominal vs. Peripheral Obesity
Large Insulin-Resistant
Adipocytes
Menopause
Small Insulin-Sensitive
Adipocytes
Android Obesity
Sharma 2002
Gynoid Obesity
Link between abnormalities in WAT (white adipose tissue)
and other organs and diseases associated with obesity
Biochem. J. 2010;430:e1-e4
Quality of Life for Obese*
Children and Adolescents
Obesity Predicts Depression:
Prospective Data
How did her Obesity develop?
Pathogenesis of Obesity
• Secondary causes e.g. Cushing’s rare
• Is primary obesity due to:
Energy intake or energy expenditure?
• Under-reporting of intake is common
– Obese by 34-54%
– Lean subjects 0-20%
Causes of Obesity:
Do you like Angie?
Sloth
X
Gluttony
Riotous living
Are Genetic Factors the Cause of Obesity?
• Genes vs. shared environmental influences
• Polygenic and not Mendelian: seen in twin
studies
• SNPs in FTO, MCR4
• Effect is small, and heredity is not destiny
• Monogenic syndromes are rare, e.g. PraderWilli, Carpenter, Leptin deficiency, Alstrom
Energy Balance:
Intake vs Expenditure
C
Feedback Control of Energy Intake
• 70 kg man maintaining weight x 10 yrs: 98% accuracy
• 100 kcal/day = 10 lb/yr
• 9 kg increase over 30 yrs ~ 0.3% kcal excess
– “eating like a bird”
• After caloric loading or deprivation, animals adjust
intake to reach same weight
• Ventromedial hypothalamus
Short-term influences on food intake:
We eat for non-physiological reasons!
• Input from higher brain centres: voluntary
control, psychosocial issues, emotional factors
• Environmental factors: environmental
threats, food availability, food palatability,
energy required to obtain food
• Metabolic/autonomic input: glucose
metabolism, SNS function
• Satiety signals: gastric stretch, gut peptides
Diet has changed
Fat as the Macronutrient Culprit?
Protein
Carbohydrat
e
Fat
Energy content per g
4
4
9
Ability to end eating
High
Moderate
Low
Ability to suppress hunger
High
High
Low
Storage capacity
Low
Low
High
Pathway to transfer excess
to alternative compartment
Yes
Yes
No
Ability to stimulate own
oxidation
Excellent
Excellent
Poor
Adapted from WHO Consultation 1998
Energy density and total energy intake
is our enemy
Whopper
660 kcal
Patty 300-450 kcal
Large Fries
400 kcal
Soda
150 kcal
Total
1210 kcal
Candy bar 225 kcal
1 cookie 50 kcal
How long does it takes for you to
burn….?
Adipostatic model of weight regulation
Ghrelin, GLP-1, GIP, PYY,
Adipokines
Control of Meals
•
Scant evidence that meal initiation is
controlled by metabolic or hormonal signals
•
Best evidence is that under normal
circumstances, meal initiation is based
upon learned associations
•
Compelling evidence that meal cessation
(meal size) is controlled by preabsorptive
gut signals
If only it were so easy!
Liporex
Lipotrim
Cortislim
Relacore
Cortaway
Cortigen
Cortislender
Cortiblock, etc.
Germs That Are Good For You
Role of energy expenditure
Energy expenditure declines with ageing
Intense
exercise
Discretionary
Occupational
Sitting, coffee,
smoking
Dietary induced
thermogenesis
Basal metabolic
rate
4000
3000
2000
1000
0
70 kg, Aged 25 years
James, Ralph and Ferro-Luzzi, 1989
70 kg, Aged 70 years
Is Angie’s metabolic rate low?
Physical activity has changed:
NEAT has declined precipitously
Markers of inactivity related to
obesity incidence
% Obese
Cars/household
TV viewing (hours/week)
% of Mean of All Time Points
200
100
0
1950
Prentice AM, BMJ 1995;311:437-9
1960
1970
1980
1990
Television Watching
and Risk of Obesity
Emerging as an
important factor
with our changing
work environment
High-Tech increases Body Weight
Cellular phones and remote controls
deprive us from walking!
20 times daily x 20 m = 400 m
Walking distance lost/year
400x365 = 146,000 m
146 km = 25 h of walking
1 h of walking = 113-226 kcal
Energy saved =2800-6000 kcal (= 1 extra lump of sugar/day)
 0.4-0.8 kg adipose tissue
Rössner, 2002
We need to prescribe physical
activity and energy intake
What do you think about her weight
problems during childhood?
Does this provide insight into her
problem?
Intergenerational cycle of overweight and
obesity
Men
ELDERLY
PEOPLE
overweight
Metabolic
syndrome
overweight
Tracking
Women
ADOLESCENTS
High birth weight
Low birth
weight
followed by
rapid
weight gain
Infants
overweight
Reduced
breastfeeding
Energy-dense
diets and low levels of
physical activity
Tracking
Tracking
CHILDREN
Women
overweight
Poor nutrition
Adapted from “Challenge of obesity in WHO European Region
and strategies for response: Summary;” WHO 2007
Could any of her medications be
increasing her weight?
Drugs that cause weight gain
•
•
•
•
•
•
•
•
•
•
glucocorticoids
progestins
tricyclic antidepressants
phenothiazines
2nd generation anti-psychotics
lithium
insulin
sulphonylureas
HAART
anti-epileptic agents
Not low-dose oestrogens!
Predictors of weight gain
1.
2.
3.
4.
5.
6.
7.
8.
parental overweight
lower SES
smoking cessation
low level of physical
activity
infancy and childhood
overweight
lack of parental
knowledge of child’s
sweet eating habits
recent marriage
lack of sleep
9. stress (inc. high
cal/carb foods)
10. multiple births
11. endocrine disruptors
(phthalates)
12. gut microbiota
13. perception of body
image
14. overweight/obese
social network
15. Food policy and
security
Principle components of body weight
regulation in an obesogenic environment
Americans enjoy one of the most luxurious lifestyles on Earth:
Our food is plentiful. Our work is automated. Our leisure is
effortless. And it's killing us.
NHLBI recommendations for weight
treatment
BMI category
25-26.9
27-29.9
30-34.9
35-39.9
≥ 40
If chronic
illnesses
If chronic
illnesses
+
+
+
Pharmacotherapy
-
If chronic
illnesses
+
+
+
Bariatric surgery
-
-
-
If chronic
illnesses
+
Treatment
Lifestyle
modification
Little difference between low-carb or low-fat diets for
weight loss (48 unique RCTs with 7286 persons).
Hence, recommend any diet that a patient will adhere to
in order to lose weight.
JAMA. 2014;312:923-933.
Drug Therapy
•
•
•
•
•
chronic treatment
1st generation
modest efficacy
no long-term f/u
individuals with comorbidities
• complements but
doesn’t replace life
style modifications
• sibutramine
• dexfenfluramine
Initial responders
continue to respond;
initial non-responders
are less likely
Drug Therapy: Systematic Review
and Meta-analysis
≥ 5%
weight loss
Weight
loss cf
placebo at
1 yr
D/C due to
AE
Phentermine
- topiramate
(Qsymia)
Liraglutide
(Victoza)
Naltrexonebupropion
Lorcaserin
(Belviq)
Orlistat
(Xenical,
Alli)
75%
63%
55%
49%
44%
8.8 kg
5.3 kg
5.0 kg
3.2 kg
2.6 kg
++
++
+
+
+
JAMA. 2016 Jun 14;315(22):2424-34.
Types of bariatric surgery
1
2
3
In the last 50 years there has been a steady increase in population
obesity in both developed and developing countries.
4
5
6
Covid 19 has raised new concerns for obese persons as there is an
increased likelihood of hospitalization; symptoms appear to be more
severe and there is a higher risk of mortality. Obesity already carries
increased risk for non-communicable diseases and covid morbidity and
mortality also appears higher in these populations.
The social, behavioural and environmental changes that accompany the
pandemic may also be contributing indirectly:
Work from home, school from home, business closures, physical
distancing can lead to reduced physical activity, and reduced energy
expenditure.
Food intake patterns are likely changed – affecting the quality of food
being consumed, such as dependence on restaurant prepared or readyto-heat/eat foods. The timing and amount of foods being consumed
may also be affected with more work- and school-from-home.
There is heightened marketing of unhealthy foods and beverages by the
food industry; consumers hoarding of food for storage (foods that are
processed and pre-packaged).
Healthy habits may also change such as increased in home-cooking,
fresh fruits and vegetables from increased marketing by agriculture.
Increased food security as food shortage and quality may be low for
7
vulnerable groups, especially school children who are dependent on school
meals. Job losses and added restrictions on movement in elderly population
may increase the likelihood of food insecurity.
7
Determining whether a patient needs to gain, lose or maintain weight is
dependent on several factors, some of which are listed here.
8
Before deciding the necessary weight management approach it is
important to highlight the situations listed where weight loss is
contraindicated.
9
Addressing personal behaviours, beliefs, attitudes and practices are
necessary before you as the physician should consider treating obesity.
10
An office environment should be designed to accommodate overweight
and physically challenged patients.
Examine the physical space, staff, instruments and overall
receptiveness of the treatment space.
11
Studies show health professionals either do not properly identify, advise
or make appropriate referrals for obese patients.
Generally, health professionals perceptions consider obese patients
behaviours as being personally responsible for their obesity.
From the patient standpoint, it is important to understand the reasons
for weight loss and the readiness of the patient. This will help to
determine the success of carrying out the necessary therapeutic steps.
12
What are your attitudes towards body size, unhealthy eating
behaviours, food safety, exposure and response to marketing and
changes in the environment.
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
Johnson Stoklossa C and Atwal S. Nutrition Care for patients with
weight regain after bariatric surgery. Gastroenterology research and
Practice 2013;2013:1-7
56
57
58
59
60
61
62
The Metabolically Stressed Patient
Dr. Carolyn Taylor-Bryan
Objectives
• The stress response
• Mediators of the stress response
• Metabolic alterations during stress
• Determination of nutrient requirements in stress
The Metabolically Stressed Patient
• Stress responses to surgery, trauma, sepsis & critical
illness
• Network of physiologic responses employed by the
organism in an effort to survive
• Complex interactions of numerous mediators - nervous
system input, hormones & cytokine messengers
• 55 yo male post surgery for incarcerated gangrenous
inguinal hernia.
• D5 post op had anastamotic leak with intra abdominal
sepsis. Abdomen is firm and distended and he does not
pass flatus.
• Temp = 39.5 C, ↑ WBC count
• In ICU, requiring ventilatory suport
The Metabolically Stressed Patient
Duration & severity of metabolic responses depend on:
-
degree of insult
persistence of insult
host response
nutritional status of host
timing in relation to previous insults
The Metabolically Stressed Patient
• Nutritional intervention utmost importance
• Difficult to provide:- alterations in nutrient utilization
- limitations of nutrient delivery associated with critical
illness
Stress response
Liberate stored nutrients & substrates to support the
healing process & endogenously nourish the organism
 Oxidative fuel
 Synthesis of building blocks – organ function
 Maintenance of immuno-competency
 Repair of injured tissue
Stress response - byproducts
fluid & sodium
overload
hypermetabolism
persisent LBM
wasting
hypercatabolism
glucose
intolerance
Stress response
LOCAL RESPONSES – collagen synthesis, matrix
protein synthesis, wound repair
SYSTEMIC RESPONSES – altered protein synthesis,
↑ nitric oxide synthase, ↑ leucocyte endothelial cell
adhesion molecules
Stress response
• Ebb phase
• Acute or flow phase
Stress response
EBB PHASE
•
•
•
•
Immediately after injury
Lasts ~24-48h
↑ in sympathetic activity
Hypometabolism + ↓ oxygen consumption
As a result of ------ hypovolemia leading to ↓ cardiac output
& inadequate oxygen transport to the tissues
Stress response
ACUTE OR FLOW PHASE
• Hypermetabolism ( ↑REE, ↑temp), catabolism, ↑ O2
consumption, , ↑ cardiac output
• Mediated by cytokines, hormones & afferent nervous
signals from injured tissues
Stress response
ACUTE OR FLOW PHASE
• Active liberation of endogenous substrates
- glycogen-derived glucose
- skeletal muscle-derived & labile aa
- adipose tissue fatty acids
• Duration a function of insult but peak 3-4 d, duration
7-10 d
Stress response
Role of each substrate
• GLUCOSE – fuel for the CNS, the wound & the immune
system
• FATTY ACIDS – energy source for cardiac & skeletal
muscle, the liver & many other tissues
• AMINO ACIDS – gluconeogenesis, majority for synthesis
of APP, thermogenesis & precursors for tissue repair
Mediators of the response
• Counter-regulatory hormones = “fight or flight” hormones
• Cytokines and other mediators
“Fight or Flight” hormones
Mediators of the response
Glucagon
• hepatic glycogenolysis
• gluconeogenesis
Cortisol
• glucagon secretion
• ↑ hepatic gluconeogenesis
• skeletal muscle breakdown
• stimulates lipolysis
Catecholamines
•
•
•
•
↑glycogenolysis
↑hepatic gluconeogenesis & ketogenesis
stimulates lipolysis
↑ REE
NET RESULT
•
•
•
•
↑ protein mobilization
hyperglycemia,
insulin resistance
↑ lipolysis
Mediators of the response
CYTOKINES
• ↑ levels during surgical stress & critical illness
• Endothelial cells & immune cells
• Hormonal regulators of the immune system
• TNF, IL-1, IL-6, IL-8
Cytokines
• TNF induces net catabolism state by:- ↑ catabolism
- anorexia
- activates hypothalamic-pituitary-adrenal axis
• IL-1 – high levels - fever, anorexia, ↓ intake,
- hypotension, inflammation
- accelerated protein breakdown
Cytokines
• IL-6 - acts with other cytokines synergistically,
- stimulates release of hepatic acute phase
reactants (CRP, fibronectin, antitrypsin,
ceruloplasmin)
METABOLIC ALTERATIONS
Stress – resting energy expenditure
• Decrease in REE initially,
then increased in flow
phase
Stress – carbohydrate metabolism
[Normal conditions – glucose homeostasis]
• Catabolic hormones stimulate glycogenolysis & glucose
mobilization
• Glycogen stores become depleted within 12-24h &
endogenous lipids (espc TG) become major source of
oxidative energy
• No increase in peripheral uptake of glucose
Stress – carbohydrate metabolism
• Hyperglycemia – characteristic finding
• Maximum rate of glucose oxidation in metabolically
stressed adults is 4-6mg/kg/min
• Provision of glucose greater than this rate results in
hyperglycemia, hepatic steatosis, lipogenesis
Stress – protein metabolism
• Protein breakdown & synthesis both continue to occur at
accelerated rates, pt remain in net negative N2 balance
• Proteolysis exceeds protein synthesis ( skeletal muscle,
connective tissue & unstimulated gut)
• aa needed for synthesis of APP, tissue repair, hormone
synthesis, immune function (cytokines,Ig )
• Results in ↑ urea excretion
↓ LBM
Stress – protein metabolism
• While positive APP production is increased, production
of most hepatically synthesized proteins such as albumin
& transthyretin, falls
• Patients who receive adequate exogenous aa to
maintain production of APP & other important hepatic
proteins are more likely to survive
Stress – protein metabolism
• Protein catabolism persists despite the provision of
apparently adequate nutrition support
• As protein catabolism increases, synthetic processes fail
to keep up with breakdown rate resulting in severe
losses of skeletal & visceral protein
Stress – protein metabolism
Prolonged catabolism of skeletal muscle protein
•
•
•
•
compromise respiratory function
impairs wound healing
exacerbates immunosuppression
accelerates the loss of strength & endurance necessary
for recovery
• ↑ risk of death
Stress – fat metabolism
• ↑ rate of FA oxidation as a result of ↑ lipolysis
• Free FA are released into the plasma at a rate far
exceeding their oxidation
• Excess FA undergo hepatic re-esterification, with
resultant accelerated hepatic TG formation
• Clinical picture of essential FA develops
Stress – fluid & electrolyte homeostasis
• Positive water balance
• Weight gain
• Positive sodium balance
• Fluid retention (extravascular space)
Critical illness
Critical illness
REE
Normal or 
initially then 
Glucose utilization

Fatty acid utilization

Ketone utilization

Gluconeogenesis

Muscle protein
catabolism

Determination of nutrient requirements
in stress
Aim - to provide the basics of nutritional & metabolic
support
- adequate fluid resuscitation
- appropriate protein, calorie & micronutrient
administration
- early enteral feeding desired
- enteral vs parenteral nutrition
Determination of nutrient requirements
in stress
ENERGY EXPENDITURE
• Clinically difficult to estimate caloric needs of critically ill
patient
• Ideally – measured by indirect calorimetry
Determination of nutrient requirements
in stress
ENERGY EXPENDITURE
• Estimating TEE
- multiply BEE (Harris-Benedict equation) by a stress
factor
- provide ~ 25-30 kcal/kg/d as maintenance
• Excess calories may ↑ CO2 production, compromising pt
with respiratory insufficiency
Increase in BEE
Determination of nutrient requirements in
stress
CARBOHYDRATES
• Glucose infusion rate - ≤ 5mg/kg/min
• ~ 50-60% of total energy requirement
• Close monitoring for hyperglycemia
Determination of nutrient requirements in
stress
PROTEIN
• 15-20% of total nutrient intake or 1.5-2.0 g/kg/d
• Protein > 2g/kg/d has not been beneficial, in fact may
result in azotemia
Determination of nutrient requirements
in stress
FATS
• 10-30% of total energy requirements
• Minimum of 3-5% of total energy as EFA to prevent
deficiency (TPN)
• Complications – hyperlipidemia, coagulopathies,
impaired immune function
Determination of nutrient requirements
in stress
FLUIDS & ELECTROLYTES
• Fluid & salt retention
• 15-20% increase in the expansion of the extracellular
fluid space
• Altered electrolyte levels can impair organ function
(dysrrythmias, intestinal ileus, impaired mentation)
• Adequate urine output & normal serum electrolyte
concentration with emphasis on intracellular K, P, Mg
Determination of nutrient requirements
in stress
VITAMINS & MINERALS
• Estimated ↑ micronutrient requirements during stress &
sepsis due to ↑ metabolic demands
• No specific guidelines regarding vitamin & mineral
requirements in critically ill
• Ensure recommended dietary allowance
Immunonutrition
• Critically-ill patients experience
- an extent of hyperinflammation
- cellular immune dysfunction
- oxidative stress
- mitochondrial dysfunction
• On-going research supports the use of specific nutrients
to modulate the immune and/or metabolic response
Determination of nutrient requirements
in stress
IMMUNE ENHANCING DIETS
• Most common nutrients in currently available enteral
immune-modulating formulas are:
- omega-3 fatty acids (EPA, DHA)
- nucleotides
- arginine
- antioxidants
- glutamine
Determination of nutrient requirements
in stress
IMMUNE ENHANCING DIETS
• Meta-analyses of trials of “immune enhancing” enteral
diets containing, glutamine, branched chain aa , omega3 FA, RNA & trace elements in critical illness concluded
that these diets reduced the risk of infection, ventilator
days & hospital length of stay without influencing
mortality
Omega-3 fatty acids
↑ omega-3 to omega-6 ratio reduces
proinflammatory products
Nucleotides
Enhances humoral immunity &
macrophage activity
Arginine
Enhances phagocytosis, protein
synthesis, production of NO
Glutamine
Primary oxidative fuel for small bowel
mucosa, lymphocytes & macrophages
Determination of nutrient requirements
in stress
ANTIOXIDANTS IN SEPSIS
• Free radical
- production is higher during infection and sepsis
- may injure cell membranes directly or may damage
intracellular proteins, nucleic acids and organelles
leading to cell death
• Carotenoids, selenium & vitamins A, C and E - protective
Feeding the patient
3 developments enabling virtually all hospital pt to be fed
safely
• Technique of central venous cannulation & infusion of
hypertonic nutrient solutions into the SVC
• Specific enteral formula diets (feeding tube)
• Availability of fat emulsion for safe iv administration
Feeding the patient
• When it is anticipated that critically ill pt will be unable to
meet their nutrient needs orally for a period of 7-10d
• Enteral nutrition preferred to parenteral nutrition
• Parenteral nutrition reserved for patients in whom enteral
nutrition is not possible
Conclusion
• Development of malnutrition is rapid in critically ill &
septic pt due to the complex metabolic changes induced
by mediators & hormones
Conclusion -Stress response in critical illness
STRESS PHASE
• Goal – resuscitation + metabolic support (permissive
underfeeding – supporting cellular metabolic pathways
without compromising organ structure and function)
CATABOLIC PHASE
• Goal – provide ongoing metabolic support with high
protein feeding while avoiding overfeeding
ANABOLIC PHASE
Goal – nutrition support for repletion of LBM + fat stores
Case
AB is a 65 y.o. female who was having breakfast with RH, a
24 y.o. female at the time of the earthquake. AB who was
30% above her IBW was rescued 20 hours after the
earthquake. She received multiple fractures of both legs
and of her left arm and has possible internal injuries from
blunt trauma. RH was rescued 30 min after the earthquake
with no injuries.
How has the trauma altered the metabolism of AB
compared to the metabolism of RH?
• 55 yo male post surgery for incarcerated gangrenous
inguinal hernia.
• D5 post op had anastamotic leak with intra abdominal
sepsis. Abdomen is firm and distended and he does not
pass flatus.
• Temp = 39.5 C, ↑ WBC count
• In ICU, requiring ventilatory suport
Increase in BEE
Energy requirements
*healthy well-nourished adults
TDR
=
BMR
+
(60-75%)
EEA
(15-30%)
+
TEF
(~10%)
TDF = total daily requirements
BMR = basal metabolic rate
EEA = energy expenditure of activity
TEF = thermic effect of food
* nutritional repletion, childhood, pregnancy, ill
- BMR varies
Thank you
MANAGEMENT OF CACHEXIA &
EATING DISORDERS
Dr Carolyn Taylor-Bryan
Cancer cachexia

Cachexia vs anorexia

Etiology of weight loss

Nutritional alterations

Mediators of cachexia

Principles of management
Cachexia -definition
Syndrome consisting of:




Lack of energy / weakness
Wasting (unintentional loss of >5-10% of body
weight)
Progressive impairment of vital functions
Severe reduction in muscle mass, loss of subcutaneous
fat, pale atrophic skin, anemia, potassium deficiency
Cachexia

Cancer

AIDS

Hyperthyroidism

Chronic obstructive pulmonary disease

Kidney disease

Congestive heart failure
CANCER CACHEXIA
Cancer

Nutrition support - integral part of care

Cachexia in 60-70% of patients - increased morbidity &
decreased quality of life & survival

Highest rates of malnutrition among hospital patients
Anorexia - definition

Loss of desire to eat, which frequently leads to reduced food
intake
Cancer anorexia-cachexia

Anorexia & cachexia can co-exist

Muscle wasting occurs even in the presence of a normal food
intake

Increased muscle proteolysis is detectable even before weight
loss occurs

When anorexia accompanies cachexia it acts synergistically to
impact on patients’ morbidity, mortality & quality of life
Tumor type and prevalence of malnutrition
Cancer cachexia – etiology of weight loss
1. ALTERED INTAKE

Direct involvement with GIT function & physiology

Depression


Modalities to Tx cancer (chemo, radiotherapy, surgery –
radical resection of stomach)
Alterations in taste (Tx, nutrient deficiencies)
Cancer cachexia – etiology of weight loss
2. DECREASED ABSORPTION



Tumor involvement of GIT – mechanical obstruction with
decreased absorption & diarrhea
Partial / complete bowel obstruction → stasis → bacterial
overgrowth → interferes with absorption of nutrients
Gastric & pancreatic resection – malabsorption of fats &
protein
Cancer cachexia – etiology of weight loss
DECREASED ABSORPTION

Small bowel / colon resection – absorption of nutrients, fluid &
electrolytes

Mucositis, nausea, vomiting, ileus (chemotherapy)

Enteritis, mucosal inflammation, intestinal fibrosis, stricture
(radiation)
Cancer cachexia – etiology of weight loss
3. ALTERED METABOLISM




Increased catabolism
Tumor – proteolysis inducing factor, lipid mobilizing factor
Cytokines
Hormones – insulin resistance
Nutritional alterations in cancer cachexia
ENERGY EXPENDITURE




Elevation in metabolic rate not seen uniformly in all cancer
patients
↑ in REE parallels advanced disease & ↓ food intake
Tumor specific
Largest increases - with lung cancer, gastric cancer and
sarcomas
Nutritional alterations in cancer cachexia
CARBOHYDRATE METABOLISM

↑ gluconeogenesis

Glucose intolerance observed in ~60% of cancer pt
Nutritional alterations in cancer cachexia
LIPID METABOLISM


Fat mobilization with losses of fat stores - ↑lipolysis & fatty
acid oxidation
Products of lipolysis (glycerol & FA) provide substrates for
gluconeogenesis
Nutritional alterations in cancer cachexia
PROTEIN METABOLISM


Progressive reduction of skeletal muscle mass – releases
gluconeogenic aa
Whole body protein turnover, protein catabolism & nitrogen
excretion are increased - ↓LBM

↓ muscle protein synthesis

Visceral protein reserves preserved
Mediators of cachexia

Cytokines are mediators of inflammation, injury & repair

Secreted by macrophages & lymphocytes in response to tumors

TNF, IL-1, IL-6, interferon gamma
CYTOKINES




TNF - ↑ lipolysis, inhibits lipoprotein lipase – results in
hypertriglyceridemia
IL-1 – fever, anorexia, ↓ intake
IL-6 - acts with other cytokines synergistically –mediates
cachexia
Interferon gamma – inhibits lipoprotein lipase & acts
synergistically with TNF to produce cachexia
CYTOKINES






Creates a hostile environment for pathogens
↑ body temperature & REE
Stimulate oxidant production
Stimulate immune system
Release endogenous substrate from muscle, skin, bone &
adipose tissue via hormones
aa release from muscle, protein oxidation, lipolysis,
gluconeogenesis, glycogenolysis
CYTOKINES
Consequences

Wasting

Increased nitrogen losses

XS cytokine production →↑ mortality

Poor antioxidant status → XS cytokine production →
increased mortality
Cancer cachexia – principles of management



Optimal therapy for anorexia & cachexia - curing the
underlying cancer
Aim of nutritional support – halting of nutritional decline and
delay or prevent the development of malnutrition
Early nutritional intervention is essential to improve prognosis
and outcome – preventing onset of malnutrition & the vicious
cycle
Cancer cachexia – principles of management


Weight loss may persist despite provision of adequate calories
& protein because of the progression of the disease / effects
of cytokines
Hypercaloric feeding – not shown to promote weight gain
Cancer cachexia – principles of management







Optimize intake
Nutrition counseling – individualized
Maintenance energy requirements ( those without weightt loss)
Higher energy provision optimize weight gain (those with
weight loss)
Protein needs vary with catabolic state
Repletion of vitamin & trace element status
? Oral vs enteral vs parenteral route
Cancer cachexia – principles of management
ORAL FEEDING



Oral intake whenever possible
Meal preparations – frequent small meals, energy dense,
presentation of food, avoid high-fat foods (exacerbate early
satiety & delays gastric emptying)
Oral nutritional supplements (↑ nutrient intake)
Cancer cachexia – principles of management
SPECIALIZED NUTRITION SUPPORT (SNS)

Bypassing oral intake to overcome cancer cachexia syndrome
related anorexia

Enteral or parenterl nutrition

Pre-op SNS may be beneficial in moderately or severely
malnourished pt if administered for 7-14d pre-op
Cancer cachexia – principles of management
ENTERAL NUTRITION

Unable to meet nutritional needs by oral intake

Terminal patients who are no longer candidates for Tx

Has been shown to increase appetite, energy & protein intake
in cancer patients
Cancer cachexia – principles of management
PARENTERAL NUTRITION

Enteral management is not feasible or is inappropriate & at
risk for becoming malnourished

Parenteral nutrition - unlikely to benefit patients with advanced
cancer whose malignancy is documented as unresponsive to
chemotherapy or radiation therapy
Cancer cachexia – principles of management ADJUNCTIVE APPROACHES
Nutritional supplements with anti-inflammatory properties

EPA (eicosapentanoic acid)
- fish oil
- down regulatory effects on pro-inflammatory
cytokines and proteolysis inducing factor
- increases LBM
Cancer cachexia – principles of management ADJUNCTIVE APPROACHES
Nutritional supplements with anti-inflammatory properties

EPA + leucine metabolite - hydroxybetamethylbutyrate
(HMB)
– animal studies
- aids protein synthesis better than EPA alone in
reversing CC
-clinical studies needed
Cancer cachexia – principles of management ADJUNCTIVE APPROACHES
Agents preventing treatment related toxicities



glutamine - ↓esophagitis in pt RT for lung CA
melatonin - ↓severity & incidence of CT
induced enteritis
octreotide – prevent CT, RT chemo-radioT
induced diarrhea
Cancer cachexia – principles of management ADJUNCTIVE APPROACHES
Appetite stimulants




Corticosteroids - ↑ appetite in GI cancers
Megestrol acetate – stimulate appetite + increase non-fluid body
mass……primarily FAT
NSAIDs + megestrol acetate – greater increase in body weight
than megestrol acetate alone
Thalidomide - potent inhibitory action on TNF-œ
Cancer cachexia – principles of management ADJUNCTIVE APPROACHES
Appetite stimulants


Ghrelin – a growth hormone secretagogue – stimulates food
intake, adiposity & weight gain
Androgenic steroids – nandrolone decanoate + CT – less
weight loss cf CT alone

42 y female, metastatic gastric cancer with gastric outlet
obstruction. Had bypass surgery (palliative).

Nutritional support – aggressive or palliative ?

Oral or enteral or parenteral nutrition ?
Conclusion

Cancer cachexia – common problem in large proportion of
patients

Cancer related anorexia & cachexia adversely affects patient
outcome – associated with poor response to treatment against
cancer

Current treatment for CC principally depends on its prevention
rather than reversing the disease state
Conclusion

Prevention of treatment related morbidities – nausea, vomiting,
mucositis, pain, depression may positively impact the patients
QoL and treatment against cancer itself and related cachexia
Reading material

Laviano et al Nat Clin Prac Oncol 2005;2(3):158-165
EATING DISORDERS
Objectives
Anorexia nervosa / Bulimia nervosa




Definition
Epidemiology
Etiology
Clinical features
Case presentations

A 16 yo girl who initially was underweight has been dieting &
lost 20lbs in the last 3 months

A 19yo girl has been sent home from college because she was
found vomiting every night in her dormitory room

A 14yo boy has been exercising 3 hours a day & eliminated
all fat from his diet to “increase my muscle mass and decrease
my fat”
Case presentations

An 11yo girl has grown 2 inches but gained no weight since
her last check- up 1 year ago

A 15yo girl is found to have empty boxes of laxative hidden
under her bed but denies they are hers
Eating disorder - definition


Persistent disturbance of eating behavior or a behavior
intended to control weight, which significantly impairs physical
health or psychosocial functioning and is not secondary to a
general medical condition or another psychiatric disorder
Best recognized eating disorders
- anorexia nervosa
- bulimia nervosa
- eating disorder not otherwise specified
ANOREXIA NERVOSA
“a nervous loss of appetite”
Anorexia nervosa - definition
Diagnostic criteria for Anorexia Nervosa from the Diagnostic and
Statistical Manual of Mental Disorders, fifth edition (DSM-V)
 Restriction of energy intake relative to requirement, leading to
a significantly low body weight in the context of age, sex,
developmental trajectory, and physical health.
 Intense fear of gaining weight or of becoming fat, or persistent
behavior that interferes with weight gain, even though at
a significantly low weight
 Disturbance in the way in which one's body weight or shape is
experienced, undue influence of body weight or shape on selfevaluation, or persistent lack of recognition of the seriousness
of the current low body weight
Anorexia nervosa - types
RESTRICTING TYPE
- accomplish weight loss primarily through fasting or excessive
exercise

BINGE-EATING / PURGING TYPE
- during current episode the person has regularly engaged in
binge-eating or purging behavior
- some lose control & regularly engage in binge-eating followed
by purging behaviors - some routinely purge after eating small
amounts of food

Anorexia nervosa - epidemiology

Commonest onset – mid-teens, up to 5% start in early 20’s

Lifetime prevalence 0.5-2% among women

Male: female ratio 1:10-20

Vulnerable groups – dancers, athletes (distance runners,
gymnasts), fashion modeling
Anorexia nervosa - etiology

Multifactorial

No known direct cause


Likely – interaction of several biological, psychological &
environmental risk factors
More prevalent in Western cultures
Anorexia nervosa - etiology
Genetic / familial
 Temperament / personality - perfectionism & obsessional
symptomatology
 Developmental factors
- proximity of puberty & development of
secondary sex characteristics to the usual age
of onset of AN
- psychological reactions to the maturing body,
changing peer relationships & new life challenges
 Sociocultural influences - media equates beauty with a slender,
sometimes cachectic, physique …suggests diet regimes

Anorexia nervosa - etiology
Sociocultural influences
*Negative peer influences
*Family dynamics
- intrusiveness, hostility, abnormal attachment processes – espc in
presence of ill family member
- adolescents who perceive parental caring & expectations as
low, physical / sexual abuse

*Maternal influences
- conveying her own weight & shape concerns by acting as a
role model, directly by critical comments or through
inappropriate feeding interactions
Anorexia nervosa - symptoms

Not everyone experiences all of the same symptoms and
behaviors
Anorexia nervosa - symptoms
Weight & Shape Concerns

intense preoccupation with their weight and shape

weight loss is of primary importance and it begins to take
precedence over other important life roles and responsibilities
Anorexia nervosa - Weight & shape concerns

Dramatic weight loss, or failure to make expected weight gains
during periods of normal growth (i.e. during childhood,
adolescence, pregnancy)

Excessive weighing of oneself; setting progressively lower and
lower goal weights

Other body checking behaviors such as looking in mirrors,
measuring or assessing body parts or frequently asking others
for reassurance with questions like "do I look fat?"
Anorexia nervosa - Weight & shape concerns




Changes in weight, even slight fluctuations up or down, have a
significant impact on mood and self-evaluation
Frequent comments about feeling “fat” or overweight despite
weight loss
Body distortions focused on particular parts of their body
being “fat” or too big
Excessive exercise – adhering to a rigid exercise regimen
despite foul weather, fatigue, illness or injury
Anorexia nervosa - symptoms
Food & Eating Behaviors

may seem counterintuitive, but individuals with anorexia often
spend a great deal of time thinking about, obsessing over and
even preparing food

often develop rigid food rules and become preoccupied with
thoughts of food and methods of controlling their intake (an
attempt to avoid weight gain)
Anorexia nervosa - Food & Eating Behaviors

Denial of hunger

Dieting, restricting or otherwise limiting food intake

Rigid counting/calculating of calories and/or fat grams
(sometimes via smartphone apps or other food/exercise
monitoring programs)

Refusal to eat certain foods, progressing to restrictions on
entire categories of food (e.g. no carbohydrates, no meat, no
processed foods)
Anorexia nervosa - Food & Eating Behaviors





Collecting or hoarding recipes
Cooking elaborate meals for other people but not eating the
food
Development of food rituals (e.g. eating foods in a certain
order, excessive chewing, rearranging food on a plate)
Possible use of laxatives, diet aids or herbal weight loss
products
Consistent excuses to avoid mealtimes or situations involving
food
Anorexia nervosa - symptoms
Changes in Personality and Social Behavior

often high-achieving individuals with a tendency towards
perfectionism

these personality characteristics can become heightened during
the disorder
Anorexia nervosa - Changes in personality and
social behavior





Increasing isolation; withdrawal from friends and activities that
were once enjoyed
Symptoms of depression and anxiety (this can be a sign of an
underlying co-occurring disorder or may be a biological
response to extreme low body weight)
Irritability, moodiness
Interpersonal conflicts
Defensive stance when confronted about weight or eating
behaviors
Anorexia nervosa - Changes in personality
and social behavior

Low energy and fatigue

Use of pro-Ana websites (internet groups that
promote/support anorexia)


Posting of “thinspiration” on social networking sites (images of
emaciated models used as inspiration to pursue anorexic
behaviors)
Wearing layers or baggy clothes to hide weight loss (and to
keep warm as body temperature drops)
Anorexia nervosa - symptoms

It can be very easy to confuse behaviors in the early stages of
anorexia with a simple desire to “eat healthy”, “get in shape”
or “just lose a few pounds”

Unfortunately, for people who are genetically at-risk for an
eating disorder, these seemingly harmless goals can quickly
escalate into rapid weight loss and a full blown eating
disorder
Anorexia nervosa - physical








Significant changes in their health and physical functioning
Anorexia nervosa’s cycle of self-starvation - the body is
denied the essential nutrients it needs to function normally
The body is forced to slow down all of its processes to
conserve energy
Muscle loss and weakness (emaciated)
Growth may be stunted (pre-pubertal onset)
Severe dehydration, which can result in kidney failure
Edema (swelling)
Fainting, fatigue, lethargy and overall weakness
Anorexia nervosa - physical







Dry skin and hair, brittle hair and nails, hair loss
Anemia (can lead to fatigue, shortness of breath, increased
infections, and heart palpitations)
Severe constipation (↓ GI motility)
Prepubertal patients may have arrested sexual maturity and
growth failure.
Amenorrhea (loss of menstrual cycle)
Infertility, increased rates of miscarriage and other fetal
complications
Impaired immune function
Anorexia nervosa - physical






Abnormally slow heart rate and low blood pressure
Damage to the structure and function of the heart; increased
risk of heart failure arrythmias and death
Hypokalemic alkalosis (vomiting, diuretics)
Reduction of bone density (osteopenia and osteoporosis) which
results in dry, brittle bones
Drop in internal body temperature, with subsequent growth of
a downy layer of hair called “lanugo,” which is the body’s
effort to keep itself warm
Depression, social withdrawal, increased risk for suicide
PRINCIPLES OF
MANAGEMENT
Anorexia nervosa – principles of
management

Treatment difficult

For successful Tx, pt must want to change & must have support
(family & friends)

Multidisciplinary (medical doctor, nutritionist, psychiatrist,
family)

Form relationship with patient
Anorexia nervosa – principles of
management
RESTORATION OF NUTRITIONAL STATE
Decide whether outpatient or inpatient management
- severity & rapidity of wt loss (BMI < 13.5, rapid weight loss)
- medical complications - electrolyte disturbance or other
hazardous complication
- serious depression
- suicidal ideation
- unresponsive to outpatient treatment
- patients lack of motivation for change

Anorexia nervosa – principles of
management
RESTORATION OF NUTRITIONAL STATE
Outpatient treatment
- total outpatient approach -followed by psychiatrist & team in
private setting – downside is that eating patterns cannot be
observed & activities such as bingeing & purging cannot be
monitored
- day-treatment programs – allows for closer monitoring of food
intake – group counselling


Inpatient treatment
Anorexia nervosa – principles of
management
RESTORATION OF NUTRITIONAL STATE




Oral intake of balanced diet recommended
Multivitamin & zinc supplementation (15mg elemental Zn/d)
Invasive nutrition support indicated for severely malnourished
(>30% recent weight loss or <65% of ideal body weight), pt
unwilling to ingest adequate nutrition
Enteral feeding controversial wrt ethics of placement of a tube
in an uncooperative or unwilling patient
Anorexia nervosa – principles of
management
CALORIC RECOMMENDATION




“START LOW & GO SLOW”
A.S.P.E.N guidelines - provide ~20kcal/kg/d to start or
~ 1000kcal d & keep increases in calories modest during first week
Other investigators – no more than 70% of predicted REE from
Harris-Benedict equation using actual weight
NICE & BAPEN – start feeding at 10kcal/kg/d and slowly increase
over 4-7d (if BMI< 14kg/m2 – start at 5kcal/kg/d)
Anorexia nervosa – principles of
management
RESTORATION OF NUTRITIONAL STATE



Recommended that for the first 4-6 weeks, weight gain should
not exceed 1kg/week; if weight increases more rapidly, fluid
retention is likely
Monitoring for complications such as edema, gastric retention,
constipation & cardiac complaints is required daily at first but
frequency decreases as feeding progresses
Monitoring in-patients - lab data should be monitored
frequently initially (~every d x 3d, then q 3d) until stable
Refeeding syndrome
“The metabolic & physiologic consequences
of depletion, repletion, compartmental
shifts & interrelationships of phosphorus,
potassium, magnesium, glucose metabolism,
vitamin deficiency & fluid resuscitation”
What is refeeding syndrome ?




Complications occur regardless of route of feeding (enteral or
parental)
These shifts result from hormonal & metabolic changes and
may cause serious clinical complications
Hallmark biochemical feature is hypophosphatemia
May also feature abnormal sodium & fluid balance, changes in
glucose, protein & fat metabolism, thiamine deficiency,
hypokalemia & hypomagnesemia
How does refeeding syndrome
develop ?

The underlying causative factor of refeeding syndrome is the
metabolic & hormonal changes caused by rapid refeeding,
whether enteral or parenteral
How does refeeding syndrome
develop ?
PROLONGED FASTING
 With fasting, ↓ insulin-to-glucagon ratio

Several intracellular minerals become severely depleted –
phos, Mg, K

However serum concentration of these minerals may remain
normal as they are mainly in the intracellular compartment

Increased urinary Mg excretion
How does refeeding syndrome
develop ?
REFEEDING





Primary cause of metabolic response to refeeding is the shift
from stored body fat to carbohydrate as primary fuel source
Glycemia leads to increased insulin & decreased secretion of
glucagon
Insulin stimulates glycogen, fat & protein synthesis
This process requires minerals such as phosphate & Mg &
cofactors such as thiamine
Insulin stimulates absorption of potassium into cells through the
Na-K ATPase symporter, which also transports glucose into the
cells
How does refeeding syndrome
develop?
REFEEDING




Mg & phosphate are also taken up into the cells
Water follows by osmosis
These processes result in a decrease in the serum levels of
phosphate, K & Mg, all of which are already depleted
The complications of refeeding syndrome occur as a result of
these electrolytes & the rapid change in basal metabolic rate
Refeeding syndrome

First sign of refeeding syndrome – increased RR

Have to be aware in order to detect

If detected, reduce rate of feeding & replenish essential
electrolytes
BULIMIA NERVOSA
“ox hunger”
Bulimia nervosa


A serious disorder that involves a recurring pattern of binge
eating followed by dangerous compensatory behaviors in an
effort to counteract or “undo” the calories consumed during the
binge
Often feel trapped in this cycle of dysregulated eating……..
a risk for major medical consequences associated with bulimic
behaviors
Bulimia nervosa - definition
Diagnostic criteria for Bulimia Nervosa (from the Diagnostic and
Statistical Manual of Mental Disorders, fifth edition (DSM-V)





Recurrent episodes of binge eating
Recurrent inappropriate compensatory behaviors (such as selfinduced vomiting, misuse of laxatives, fasting, or excessive
exercise) in order to prevent weight gain
The binge eating and inappropriate compensatory behaviors both
occur, on average, at least 1x/week for 3 months
Self-evaluation is unduly influenced by body shape and weight
The disturbance does not occur exclusively during episodes of
anorexia nervosa
What is a binge ?




Mild or occasional overeating does not constitute a binge
A binge is defined as eating an amount of food, that is
definitely larger than most would eat, within a relatively short
amount of time, usually considered to be a span of 2 hours or
less
The individual experiences a sense of lack of control, and they
generally feel powerless over how much or what type of food
they are eating
During a binge episode, a person may want to stop eating but
feels unable to do so despite physical discomfort and other
negative consequences of the binge
Bulimia nervosa - types

Purging type

Non-purging type
Purging – Non-purging behaviours

Typically feel very anxious or shameful after the binge

In their attempt to prevent weight gain and relieve this
discomfort they engage in harmful compensatory behaviors

Purging behaviors - self-induced vomiting and misuse of
laxatives, diuretics, or other medications

Non-purging compensatory behaviors - periods of fasting or
excessive exercise.
Bulimia nervosa - epidemiology






More common than AN
Lifetime prevalence 1-3% of women
1-3% exhibiting partial forms of the disorder
Male: female ratio of 1:10
Most present in late teens, early 20’s (more common in college
students than adolescents)
Dieting usually precedes onset of binge eating
Bulimia nervosa - etiology

Genetic/environmental - higher levels of both BN and AN in
same families, higher prevalence of childhood & parental
obesity, early critical comments by family about weight, shape
and eating

Personality & temperament - novelty seeking, impulsivity &
harm avoidance, substance-use disorders

Developmental - association between BN and a history of
sexual abuse
Bulimia nervosa – clinical features

Only 6% of people with bulimia receive treatment for their
disorder

Often goes unidentified

Common warning signs and red flags that might indicate you
or a loved one have bulimia nervosa
Bulimia nervosa – clinical features
Weight & shape concerns

Early on in the disorder, it may become apparent that an
individual’s self-worth is becoming increasingly dependent
upon weight, shape and feedback about their bodies

Thus, efforts to lose weight or change how they look become
more intense
Bulimia nervosa - Weight & shape concerns






Preoccupation with weight and body shape
Dramatic weight fluctuations up or down
Frequently or excessively weighing oneself
Changes in weight, even slight fluctuations, have a significant
impact on mood and self-evaluation
Negative and self-critical comments about one’s body/weight
Excessive exercise - adhering to a rigid exercise regimen often accompanying periods of fasting to counteract or
“prepare” for binge episodes …… “exercise bulimia”
Bulimia nervosa - clinical features
Food & eating behaviors

Most go through a period of prolonged dieting or restricted
eating before the cyclic binging-purging episodes ever begin

The diet mentality causes intense cravings that can set people
up to binge and intensifies emotional connections to food and
weight……… can be a major trigger for people who are
already at-risk for an eating disorder
Bulimia nervosa - Food & eating behaviors









Evidence of binge eating - disappearance of large amounts of food
in short periods of time or the existence of wrappers and containers
indicating the consumption of large amounts of food
Eating until the point of discomfort or pain
Frequent trips to the bathroom immediately after meals
Any consistent signs or smells of vomiting
The presence of wrappers/packages of laxatives, diuretics, enemas
Fasting, dieting, restricting or otherwise limiting food intake for a
specified amount of time, followed by increased eating/binging
Avoiding mealtimes or social situations involving food for fear of
losing control/bingeing in a public setting
Eating alone or in secret
Hiding or hoarding food
Bulimia nervosa – clinical features
Changes in personality and social behavior


The binge /purge cycle can significantly impact an individual’s
daily life as their primary focus becomes increasingly centered
on accommodating the disorder
Inconsistent meals, nutritional deficiencies and drastic
fluctuations in eating can also impact a person’s mood and
behavior
Bulimia nervosa - Changes in personality and
social behavior





Changing lifestyle, daily schedules or establishing rituals to
make time for binge-and-purge sessions (Ex: repeatedly
skipping a class after lunch or frequently leaving events right
after the meal is served)
Withdrawal from usual friends and activities
In general, behaviors and attitudes indicating that weight loss,
dieting, and control of food are becoming primary concerns
Symptoms of depression and anxiety (this can be a sign of an
underlying co-occurring disorder )
Irritability or fluctuating moods
Bulimia nervosa - Changes in personality and
social behavior






Substance Abuse
Signs of self-injury
Lying about food or making up excuses to try to hide
behaviors
Interpersonal conflicts
Defensive stance when confronted about weight or eating
behaviors
Low energy and fatigue
Bulimia nervosa – clinical features

Unlike with anorexia, individuals with bulimia often realize that
they have a problem and may feel very embarrassed or
ashamed about their behavior

Can fuel a cycle of self-criticism and the individual continues to
turn to binging/purging as a way of coping with difficult
emotions and low self-esteem
Bulimia nervosa – physical

Recurrent binge-and-purge cycles of bulimia can affect the
entire digestive system

Electrolyte and chemical imbalances in the body that affect the
heart and other major organ functions

More difficult to detect because patients are often of normal
weight and may not disclose their abnormal eating behaviors
Bulimia nervosa – physical






Severe dehydration and electrolyte imbalances - metabolic
alkalosis, hypochloremia, hypocalcemia
Arrhythmias 2◦ electrolyte abnormalities
(hypokalemia)……heart failure………..death
Fainting
Hypotension
Sores in mouth, chronically inflamed and sore throat
Non-painful swelling of salivary glands in neck and jaw areas
– “chipmunk” facies
Bulimia nervosa – physical





Decalcification of teeth, enamel loss (palatal surface of the
upper front teeth) , staining, severe tooth decay and gum
disease as a result of repeated exposure to stomach acid
Inflammation and possible rupture of the esophagus,
esophagitis
Peptic ulcers and pancreatitis
Acid reflux disorder
Potential for gastric rupture
Bulimia nervosa – physical






Calluses of knuckles (self-induced vomiting)
Edema (swelling) - large quantities of laxatives or diuretics
Chronic irregular bowel movements, constipation and other
gastrointestinal problems
Irregular or absent menstruation
Infertility, increased rates of miscarriage and other fetal
complications
Rectal irritation
Bulimia nervosa – treatment

More amenable to Tx than AN patients
Bulimia nervosa - treatment

An important part of successful treatment for bulimia involves
helping the individual interrupt the binge/purge cycle so that
they can begin to develop new coping skills and establish a
healthy relationship with food and their body.

https://www.youtube.com/watch?v=hjm3XTMEUAM
THANK YOU
Human Nutrition
Marvin Reid MB BS PhD
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Marvin Reid
• Ardenne High Alumnus
• UWI Class of 88
• PhD Community Medicine (UWI) 1999
• Postdoctoral (Baylor College of Medicine)
• Family Medicine / General Practitioner
• Leadership roles with MAJ / CCFP / WONCA (World
Organization of Family Doctors)
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
http://www.jamaicaobserver.com/news/virus-hunger-pandemic-_196396
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
http://jamaica-gleaner.com/article/commentary/20200721/stacey-aiken-hemming-effects-covid-19jamaican-diet
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
133 Kcal
THE UNIVERSITY OF THE WEST INDIES | CAIHR
150 kcal
580 kcal
www.uwi.edu/caihr
Severe Undernutrition in Children
Since the 1950’s TMRU has
managed severe undernutrition
in children in Jamaica
WHO manual for management
of severe malnutrition based on
research and clinical care done
at TMRU
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
TMRU -Mission
The mission of the TMRU is to foster an understanding of
human nutrition and metabolism as critical drivers for
human adaptation in health and disease through
research, education and clinical service.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Objectives
•
•
•
•
•
Define human nutrition
The concept of nutrition as a demand led process
The concept of requirement
Reference dietary intakes and their uses
Nutrition in Medicine
2020-08-11
THE UNIVERSITY
OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Human Nutrition
Human
Food
Metabolic
Intake
Demand
Nutrition
2020-08-11
THE UNIVERSITY
OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Environmental
Modulating Factors
• Social
• Cultural
• Disease
Intrinsic
• Metabolic set
• Genes
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Nutrition as DEMAND led
Process
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Diet
Diet
Nutrient
CHO, lipids, Vitamins, Minerals,
Trace elements.
2020-08-11
THE UNIVERSITY
OF THE WEST INDIES | CAIHR
Other
Compounds
Additives,
Contaminants
www.uwi.edu/caihr
Function of
diet
• Fuel
• Provision of specific
nutrients which
engage in chemical
reactions.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
Turnover – constant
process of synthesis and
degradation of nutrients.
www.uwi.edu/caihr
Turnover – General Model
Storage
Pool
Functional
Pool
Exchange
Pool
Oxidation
2020-08-11
THE UNIVERSITY
OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
2020-08-11
WHOLE BODY
PROTEIN
TURNOVER
THE UNIVERSITY OF THE WEST INDIES | CAIHR
• The overall rate at which protein is
synthesized or broken down in the
body. It is the sum of the turnovers of
all individual proteins which are being
broken down and renewed at different
rates
www.uwi.edu/caihr
Catabolic states
2020-08-11
THE UNIVERSITY
OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
2020-08-11
Enables one to identify the role of
changes in S and B rates in mediating the
protein metabolic response to various
conditions
Significance of
turnover model
Increased responsiveness –large net
effects possible by small changes in S & B
rates
Energy expensive
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Metabolic Demand
• The amount of nutrient/energy required to maintain balance
• Basal=at rest, no mental or pathological stress, no food for 12 hrs, thermoneutral
environment
• Variable component
2020-08-11
THE UNIVERSITY
OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Basal Demand
• Cellular & tissue level
• Membrane Function
• Pumps
• Transport
• Signaling
• Mechanical Work
• Substrate turnover
2020-08-11
THE UNIVERSITY
OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Variable components
•
•
•
•
Processing of dietary intake
Physical Activity
Maintaining body temperature
Growth
2020-08-11
THE UNIVERSITY
OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Meeting the demand
Metabolic Demand is continuous
• Adequate supply of nutrients
• Right place
• Right time
• Adequate amounts
Mismatch between supply and demand leads
to alteration in form and function
2020-08-11
THE UNIVERSITY
OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Poll
• What is the immediate source of nutrients for the body to satisfy its
metabolic demand
•
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Demand = continuous
Diet=intermittent hence immediate Supply =Body
Satisfying the
demand
“Goodness of fit” =closer the composition of supply is
to the composition of demand, more efficient
“Capacity to do” = size and ability
Mismatch results in
adaptation
Functional cost
2020-08-11
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Concept of requirement
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Essential vs Non -Essential
• Essential Nutrients-
• Nutrients that must be supplied by the diet.
• Hence synthetic ability not preserved
• Non-Essential –
• Nutrients that can be synthesized by the organism
• Synthetic metabolic pathways preserved
2020-08-11
THE UNIVERSITY
OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Conditional Essential & Limiting
nutrient
• Conditional Essential –
• Nutrients that can be synthesized by the organism
• However in certain physiological / pathological states synthesis is insufficient to
meet demand and supplementation from diet required
• Limiting Nutrient –
• Nutrient whose concentration controls the flow through a particular metabolic
pathway
2020-08-11
THE UNIVERSITY
OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Reference Dietary intake
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
2020-08-11
Recommended
Dietary Intakes
THE UNIVERSITY OF THE WEST INDIES | CAIHR
The amounts of essential nutrients
considered sufficient to meet the
physiologic needs of practically all
healthy persons in a specified group
and the average amount of food
sources of energy needed by members
of the group
www.uwi.edu/caihr
Reference Bodies
• USA- Recommended Dietary Allowances
• UK-Recommended Intakes of Nutrients
• FAO/WHO- Safe intakes of Nutrients
Scientific evidence + value judgment
2020-08-11
THE UNIVERSITY
OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
RDI vs Guidelines
RDI are not Dietary Guidelines
• Guidelines usually given for non-essential &
essential foods
• Nutritional adequate diet
• Prevent or treat disease and hence
evidence mainly from association studies
2020-08-11
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Uses of RDI
• Assessing diets of individuals
• Dietary assessment difficult
• Assessing the diets of groups of individuals
• Reduction in imprecision due to intra-individual & inter-individual variability
• For labelling purposes
• More convenient than absolute amounts
2020-08-11
THE UNIVERSITY
OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Nutrition in medicine
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Nutrition in Medicine
Clinical Nutrition
Nutritional management
of patients or groups
with disease
Public Health Nutrition
Health promotion
or prevention of disease
in communities
Physiological Nutrition/
Nutrition thru life cycles
2020-08-11
THE UNIVERSITY
OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Changing
Pattern of
diet &
drivers
Kearney J. Food consumption trends and drivers. Philos Trans R Soc Lond B Biol Sci. 2010 Sep 27;365(1554):2793-807. doi: 10.1098/rstb.2010.0149.
PMID: 20713385; PMCID: PMC2935122.
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Life Course
Life Course
Cancer
Promoting
THE UNIVERSITY OF THE WEST INDIES | CAIHR
Cancer
Protection
www.uwi.edu/caihr
Programming Concept : Difference in BWT by Malnutrition Diagnosis at
TMRU
Forrester et al PLOS One 2012
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Objectives
•
•
•
•
•
Define human nutrition
The concept of nutrition as a demand led process
The concept of requirement
Reference dietary intakes and their uses
Nutrition in Medicine
2020-08-11
THE UNIVERSITY
OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
Thank You
THE UNIVERSITY OF THE WEST INDIES | CAIHR
www.uwi.edu/caihr
NUTRITION AND THE
MUSCULOSKELETAL
SYSTEM
Bentley Chambers
TMRU, CAIHR
UWI, Mona
September 8, 2020
OUTLINE
• Nutrition
• Musculoskeletal system
• Diseases of the muscle and bone
• Observation
• Diagnosis
• Cause
• Treatment
• Prevention
NUTRITION
The science that
study the process by
which living
organisms take in
and use food for the
maintenance of life,
growth and
functioning of organs
and tissues
Human Nutrition, 11th Edition, Geissler &
Powers, 2005
Ministry of Health, Jamaica
MUSCULOSKELETAL SYSTEM
Composed of
skeletal muscle,
tendons, bones,
joints and ligaments
Provides
mechanical support
for the body and
permits movement
Stevens & Lowe's Human Histology, 4th Edition,
Lowe & Anderson, 2015
study.com
MUSCLE DISORDERS
smaller muscle
mass
increased intramuscular fat
more
subcutaneous fat
decreased cortical
bone mass
Age-related changes in lean mass in
thigh cross-sectional area of 2 people
with similar BMI
SARCOPENIA
Sarcopenia is loss of muscle mass and
function (strength and physical performance)
Morely et al., 2011
Derived from the Greek words, sarx (flesh) and
penia (loss), literally meaning poverty of flesh
Rosenberg, 1997
Often associated with concomitant increase in
fat mass – sarcopenic obesity
Recently classified as a disease with an
International Classification of Diseases code
(ICD-10-CM)
The definition of sarcopenia is evolving and
there are no standard method to diagnose
the disease
Two commonly used classification systems
used to diagnosed sarcopenia:
 The European Working Group on
Sarcopenia in Older People (EWGSOP)
 The International Consensus
Muscle mass declines:
~ 1 % per year after the age of 30 years
~ 5 % to 13 % in persons 60 to 70 years of age
~ 11 % to 50 % in persons 80 years and older
Muscle strength and the life course
Age Ageing 2019; 48(1):16–31,
Selected factors that affect maintenance of
muscle mass with advancing age
Encyclopedia of Exercise Medicine in Health and Disease 2012; pp 775-779
Genetic and lifestyle factors can hasten muscle
weakening and progression toward functional
impairment and disability
Interventions including nutrition and exercise training
seem to slow or reverse these processes
Preventing or delaying sarcopenia, the aim is to
maximise muscle in youth and young adulthood,
maintain muscle in middle age and minimise loss in
older age.
Consequences of sarcopenia
Decreased Resting Energy Expenditure
Decreased Insulin sensitivity
Sarcopenia is considered one of the major
cause of frailty and disability in older persons
Frailty as a result of Sarcopenia increases
risk of falls and fractures and increase risk of
death
Results from chronic
inflammation associated
with age and is gradual
loss of skeletal muscle
tissue
Ageing 2011; 3(8): 702-715
Results from inflammation
associated with a primary disease
(e.g. cancer, AIDS, and sepsis) and
occurs as an acute loss of skeletal
muscle tissue
The role of diet
High rate of low dietary quality among elderly
(Robinson et al., 2019)
Results in lower intake of energy, protein and
other nutrients
Age-related changes in sensory perception,
poor oral health and impaired appetite lead to
reduced size, reduced frequency of meals
and reduced options in choice of food
Age-related
changes in
sensory
perception
impaired
Appetite
poor oral
health
meal size
frequency of meals
options in choice of food
dietary quality among elderly
intake of energy, protein and other nutrients
Low food consumption can lead to
insufficient energy intake resulting in
depletion of stored fat and catabolism of
muscle which leads to reduced muscle mass
(Carbone et al., 2012)
Intervention studies have shown
improvement in muscle mass, muscle
strength and physical performance after
protein supplementation
More significant improvements when protein
supplementation is complemented by
resistance exercise
(Tieland et al., 2012; Park et al., 2018; Cermak et al., 2012)
Calcium, potassium, sodium
Important in maintaining
healthy muscle and nerve
activity
Magnesium
Improve muscle
function and relaxation
phosphorus
Deficiency associated
with muscle weakness
Iron
Inadequacy
associated with Poor
physical performance
Zinc
delays disuseinduced muscle
atrophy
Selenium
deficiency is associated
with several muscular
diseases
Measurement of Muscle Mass
Appendicular Skeletal Mass (ASM)
- Mass of the muscle of the limbs
- Commonly used as a proxy for muscle
mass
Lean Body Mass (LBM)
- Mass of all organs except body fat,
including bones, muscles, blood, skin, etc.
- Lean body mass and fat free mass may
be used as proxies for muscle mass
STABLE ISOTOPE METHOD
Deuterium dilution
Single oral dose of deuterium oxide (D2O)
given as a tracer for total body water (TBW)
D2O equilibrates with TBW in adults by about
3 hours post dose
Samples of saliva or urine are usually
collected at 3 hours and 4 hours post dose
 TBW is determined by analyzing the
samples for deuterium enrichment using
IRMS or FTIR
 Fat free Mass (FFM) is derived from TBW
based on known age and sex specific
hydration factors of FFM
Introduction to Body Composition Assessment Using the Deuterium
Dilution Technique with Analysis of Saliva Samples by Fourier Transform
Infrared Spectrometry, IAEA, 2010
Creatine dilution
Single oral tracer dose of D3-creatine
(dose range in humans 30-60 mg)
Absorption, distribution, active uptake
and dilution in the skeletal muscle creatine pool
Conversion to creatinine
(~ 1.7% of total creatine per day; nonenzymatic reaction; irreversible in vivo)
Single urine sample at isotopic steady
state (2-4 days in humans)
Analysis of D3-creatinine enrichment by
IRMS or LCMS to determine total-body
creatine pool from which muscle mass is
calculated
D3-Creatinine enrichment to determine total-body
creatine pool
Evans, W. Non-Invasive Assessment of Muscle Mass-Novel Method for an Old Problem 2016
IMAGING METHODS
DEXA, CT, MRI
– Whole body scan
and appendicular
skeletal muscle
mass calculated
OTHER METHODS
Bioelectrical Impedance Analysis (BIA )
– using impedance and population
validated equation
Anthropometry
– Skin fold using population
validated equations
– Mid-arm circumference
and BMI used as proxies
for lean body mass
Measurement of Muscle Function
Muscle Strength
Hand held dynamometer
Strength of extremity muscles
Strength of handgrip
Physical Performance
Short Physical Performance Battery (SPPB)
 Static balance
 Gait speed – speed to walk 3 metres
 Getting in and out of a chair
Timed Up and Go test (TUG)
6 minutes walk – distance walked in 6
minutes
European Working Group of Sarcopenia in
Older People (EWGSOP) algorithm for
sarcopenia case finding in older individuals
SARC-F is a
rapid screening
questionnaire for
sarcopenia in the
elderly
Cruz-Jentoft, J. Age and Ageing 2019; 48(1): 16–31
Treatment of Sarcopenia
Clin Interv Aging 2010; 5
BONE DISORDERS
Hip Fractures
Compression fractures
and Osteoporosis
Bone remodeling cycles
Bone is a metabolically active tissue. Although the total amount of bone tissue in an adult is relatively static,
there is continuous turn over (formation by osteoblasts and resorption by osteoclasts) of bone mineral and
organic matrix. About 5-10 % of existing bone is replaced through remodeling each year.
Calcium balance by ingesting 1000 mg
of calcium per day
{total Ca ingested = total Ca excreted}
Encyclopedia of Food Sciences and Nutrition (Second Edition) 2003; pp 771-779
7-dehydrocholesterol in skin exposed to UVB
(cholecalciferol)
(25-hydroxy vitamin D3)
Ergocalciferol in plants exposed to UVB
(ergocalciferol)
(25-hydroxy vitamin D2)
25-
(1,25-dihydroxy vitamin D3)
(1,25-dihydroxy vitamin D2)
Calcium Homeostasis
Song, L. Adv in Clin Chem. 2017; 82
Bone mass during adolescence





Gain in bone mass during adolescence.
Yearly increase in spine bone mineral content (L2-L4)
during adolescence in females (○) and males (•).
Maximum bone density gain in mid-adolescence.
Soyka, L. A. et al. J Clin Endocrinol Metab. 2000; 5: 3951-3963

Dietary calcium
Physical activity
Protein-energy
malnutrition
Micronutrients
Hormones
 sex steroids
 growth factors
Genetics
Deterioration of efficiency of calcium
handling after the menopause
Premenopausal

Treated
postmenopausal
0
Ca
balance
(g/day)
Average
Ca intake :
_
Untreated
postmenopausal
0.03
0.5
1.0
1.5
Ca intake (g/day)
Heaney, R. et. al. J Lab Clin Med.
1978; 92(6): 953-953
500 mg/dy
Nutritional factors associated with
bone loss






Sodium – excess is associated with
hypercalciuria
Protein energy malnutrition  urinary loss of
Calcium
Alcohol – toxic effect, hypercortisolaemia
Caffeine – hypercalciuria
Phosphorus – diet high in phosphorus and low
in calcium reduces serum calcium
Micronutrients (Mn, Cu, Zn, vit C, vit K) –
deficiency associated with low bone density
Physical activity

Immobilization stimulates resorption
e.g. 2-9 weeks bed rest

Bone loss ~3%/month in weight bearing
bones during weightlessness

Strenuous activity associated with
increased BMD in athletes (probably most
effective during youth)
Vitamin D deficiency
(rickets and osteomalacia)
• Rickets - soft and/or weak
bones in children
• Osteomalacia – soft and/or
week bones in adults
• Caused by insufficient vitamin
D, calcium or phosphorus
• Limited sunlight exposure,
decreases serum vitamin D,
can also lead to rickets
Copyright by MRC
• Growth plates do not calcify properly, bend
more easily
• Bowed legs in young children since the
weight-bearing bones are relatively weaker
• Not all forms severe and some children with
rickets can present without the typical skeletal
phenotype
Epidemiology of rickets
J Pediatr. 2000;137:153-157
Metabolism 1991;40: 209-213
• Rare in the developed countries
• Increased awareness and improved nutrition
• Milder forms exist in persons with inadequate
calcium, phosphorous or vitamin D intake
• US infants who are breastfed solely are at
increased risk
• Some studies reveal a higher incidence in
persons of darker skin pigmentation
• Decreased dairy consumption may contribute to
the mineral deficiency in Nigerian children,
leading to increased reports of rickets
Clinical presentation



Bone pain and tenderness are common
Increased risk of bone fractures
Skeletal deformities
 Tibia - bowing of the legs
 Spinal deformities - scoliosis or kyphosis,
asymmetrical skull (craniotabes) in infants
Chest deformities - rachitic rosary (overgrowth
of cartilage at costochondral junction), pigeon
breast deformity (respiratory muscles pull on a
weakened rib cage)
 Dental deformities common in children
(delayed eruption, weaker teeth, caries)

Differential diagnosis









Osteomalacia
Osteodystrophy
Hyperparathyroidism
Malnutrition
Malabsorptive disorder
Metaphyseal chondrodysplasia
Renal tubular disorder
Treatment
Supplementation with calcium, phosphate or vit D
Orthopedic surgery for severe skeletal deformities
Osteoporosis
A skeletal disorder characterized by
compromised bone strength
predisposing a person to an increased
risk of fracture.
National Institutes of Health (USA)
Consensus Development Panel on Osteoporosis
Prevention, Diagnosis, and Therapy, 2001
Bone density
Bone quality
Micro-architecture
Normal bone
Osteoporosis bone
3250
Projected to
reach 3.250
million in
Asia by 2050
629
1950 2050
1950 2050
1950 2050
100
Total number of
hip fractures:
1950 = 1.66 million
2050 = 6.26 million
600
378
400
742
668
Projected number of osteoporotic
hip fractures worldwide
1950 2050
Estimated no of hip fractures: (1000s)
Adapted from Cooper C et al, Osteoporosis Int, 1992;2:285-289
Falls and Fractures among the elderly in
Jamaica
 From a study done in Jamaica, 1 in 5 elderly
persons reported falling in a 6 months period
(Mitchell-Fearon et al. 2014)
 79 % of falls among elderly Jamaicans resulted in
at least one fracture (James et al. 2007)
 Medical cost due to these falls, excluding room
& board was USD 9,500 per person (James et al. 2007)
Female Life Expectancy
National Vital Statistics Reports.; US Dept. of Health and Human Services,1999; 47(28).
1 year morbidity after a fracture
Patients(%)
80
40
30
20
Death within 1
yr
Am J Med 1997; 103: 12S-17S
Permanent
disability
Cannot walk
independently
Unable to carry
out 1
independent
ADL
Screening for osteoporosis using dual x-ray
absorptiometry (DXA) or calcaneal BMD
WHO classification
Non-modifiable Risk Factors
for Osteoporosis

Family history

Race: Asian or Caucasian

Advanced age

Being female

Low body weight <127 lbs (<57.7 kg)
Modifiable Risk Factors
for Osteoporosis










Cigarette smoking
Excessive use of alcohol
Insufficient calcium and vitamin D intake
Inadequate physical activity
High sodium diet
Protein malnutrition
Caffeine
Oestrogen or testosterone deficiency
Chronic use of steroids
Frailty, poor vision, recent falls, dementia
Predisposing Conditions
for Osteoporosis

Endocrine
 Cushing’s syndrome

Hyperthyroidism

Oestrogen or
testosterone deficiency

Hyperparathyroidism

Anorexia nervosa

Type 1 diabetes

Renal
 Renal failure or
insufficiency

Hypercalciuria
Predisposing Conditions
for Osteoporosis

Rheumatologic
 Ankylosing spondylitis
 Rheumatoid arthritis

Gastrointestinal
 Gastrectomy
 Malabsorption
 Liver disease
 Anticonvulsant drugs

Depression
Osteoporotic Fractures – causes
and prevention
Nothing
Menopause
Aging
Oestrogen
replacement
Increased bone loss
(bone resorption > bone formation)
Propensity
to fall
Modify
environment
FRACTURES
Low peak
bone mass
Modify lifestyle
during youth
High bone
turnover
Medications for
chronic diseases
Calcium plus Vitamin D Supplementation and
the Risk of Fractures
Among healthy postmenopausal women, calcium (800 mg) with
vitamin D (400 IU) supplementation
resulted in a small but significant improvement in hip bone
density, did not significantly reduce hip fracture, and increased
the risk of kidney stones
N Engl J Med. 2006;354:669-83
Candidates for
Osteoporosis Treatment
Guidelines for treatment therapy:
T-score below -2.0 in the absence of
risk factors
 T-score below -1.5 if other risk factors
are present
 All menopausal women who present
with vertebral or hip fractures

National Osteoporosis Foundation (NOF), 1998 guidelines.
Diagnosis of osteoporosis:
clinical evaluation





Medical history
 Risk factor assessment
 Signs and symptoms
Bone mineral density (BMD) testing
Physical examination
Laboratory tests, as appropriate
Height assessment
Recommended Daily Intake of Calcium
Age
Recommended Calcium
Intake (Daily)
9-18 years
1300 mg
19-50 years
1000 mg
51 years or older
1200 mg
The Dietary Reference Intakes (DRIs) for calcium
established by the National Academy of Sciences
Lancet 2007; 370: 657-66
Reduction of Nonvertebral Fracture with
Calcium and Vitamin D
Vitamin D Especially important in temperate countries
14
Placebo
12
Calcium + Vitamin D
500 mg/700 IU
10
%
Fracture
8
6
4
2
0
6
12
18
24
Months
N Engl J Med. 1997;337:670
30
36
Role of Exercise

Strength-training exercise can maintain or
increase BMD and improve muscle mass,
strength, and balance, decreasing risk of hip
fracture. Exercise must be tailored for individual

Studies have demonstrated a protective effect of
previous physical activity on the risk of hip
fracture

Caution is urged when prescribing specific
exercises for osteoporotic patients to avoid injury
Prevention of osteoporosis:
General recommendations

Calcium: at least 1200 mg/day from diet or
supplements

Vitamin D 400 – 800 IU/day

Weight-bearing exercise: > 30 min/3 x week

Avoidance of tobacco products

Moderation of alcohol intake

< 4 cups of caffeine/day