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Transcript
Health Education 345
Health Promotion and
Disease Prevention
Lecture notes
Spring 2010
Dr. Gordon Chalmers
Dept. of PEHR
Western Washington University
 2010, Gordon Chalmers, Ph.D.
Communicable Diseases
VOLUME 3 ISSUE 12 September 15, 2006
Wash your hands
Does it work?
Just 30 seconds of simple handwashing with soap and water reduces the bacterial count on health care
workers’ hands by 58%. And there is an even better way: Alcohol-based handrubs (discussed below)
reduce counts by 83%.
A two-year study of Navy recruits shows that handwashing pays big dividends. A simple soap and water
handwashing campaign reduced clinic visits for respiratory infections by 45%, and the sailors who washed
most often enjoyed the greatest protection.
What’s best?
Soap and water is the time-honored technique, and it does work. In fact, it’s still the best way to remove
visible soilage and particulate material. But as the public has become concerned about the risk of
infection, soaps with antibacterial additives have gradually taken over 45% of the market. It’s
understandable, but it’s not helpful; antibacterial soap is no better than ordinary soap, and the additives
actually increase the risk of allergic reactions and other side effects. The only exception is that the spores of
the anthrax bacillus are more susceptible to antimicrobial soap than ordinary soap. Unless the bioterrorism
of 2001 resurfaces, however, that’s not a worry for ordinary folks.
Plain soap will do the job — and so will plain water. Tap water is excellent, and cool or lukewarm
temperatures serve as well as hot water. In fact, excessively warm water may do more harm than good by
damaging skin.
If soap and water are not available, antibacterial wipes can help. Although they are not as effective, they will
reduce bacterial counts. Antibacterial towelettes are particularly convenient for travel and picnics.
Washing with soap and water is the best way to remove dirt, but waterless, alcohol-based handrubs
are even better at killing germs. Handrubbing is faster and more convenient than handwashing, and
it’s also easier on the skin. Hospitals are switching to handrubs because they kill more bacteria and viruses
and they are used more regularly. Alcohol-based rubs and gels are also available for use at home. The
best products contain 60%–95% isopropanol or ethanol.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 2
updated 3/17/2010
Communicable Diseases
When and how
Do it early and often.
Wash your hands before each trip to the dining room and after each trip to the bathroom. Wash after
handling diapers and animals. Wash before and after you handle food. Wash after you take out the
trash, work in the yard, clean the house, repair the car, or do other messy chores. Wash before and
after sex. Wash after you come in contact with anyone who is sick, particularly if they have a
respiratory infection or diarrhea. Wash your hands whenever they look or feel dirty, but use
common sense. If you follow reasonable guidelines you’ll be washing often, but you won’t become
obsessive or compulsive. Be careful, not fearful.
How should you wash? Liquid, bar, powdered, and lather forms of plain soap are all acceptable. Wet your
hands with water, then apply the soap to your palms. Rub your hands together briskly for at least 15
seconds before rinsing. In most cases, removing jewelry is not necessary. If your nails are dirty, scrub
under them with a nailbrush, but unless you are a surgeon preparing to operate, don’t scrub your skin.
Whenever possible, use a disposable towel to dry your hands thoroughly, and use the towel to turn off the
faucet.
Alcohol-based handrubs are preferred for health care workers, and you should consider using them at
home when dirt is not an issue but infection is a particular worry. Apply the recommended amount of the
gel or rub to the palm of one hand, then rub your hands and fingers until your hands are dry. If your
hands dry in less than 15 seconds you have not used enough rub; if it takes 30 seconds or longer,
you’ve applied more than you need.
Skin care is also important. Alcohol-based rubs are easy on the skin, but if you use a lot of soap and water,
your skin may get dry, itchy, or cracked. Soaps that contain bath oil may help, but the best protection is to
apply a moisturizer after each wash.
What is a communicable disease?
A disease that we catch from somebody (or something) else = INFECTIOUS
DISEASE.
Why are they of concern to me?
What causes communicable diseases?
GERMS = pathogens = disease causing organisms
bacteria, virus, spirochetes, protozoa, fungi (& others)
bacteria = single celled microorganism
virus = non-living particle of genetic material
spirochetes = type of bacteria
fungus = plant like microorganism
How do PATHOGENS work to make me sick?
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 3
updated 3/17/2010
Communicable Diseases
All infectious diseases follow a TRANSMISSION cycle which allows them to be passed
from one person (or thing) to the next person.
LYME DISEASE EXAMPLE
Lyme disease PATHOGEN?
RESERVOIR
supply of the PATHOGEN, a good place for it to survive, in some cases the site of
reproduction.
Lyme disease causing spirochete RESERVOIR?
other reservoirs for a variety of pathogens: animals (including people), soil, air,
water, inanimate objects = virtually everything around you (you can’t avoid
the reservoirs)
Period of COMMUNICABILITY
Time period when pathogen is most easily transmitted from the reservoir.
e.g., a cold is most easily transmitted during it’s early phases
other pathogens have specific phases when they can most likely be transmitted
(e.g., genital herpes, Most likely transmitted during outbreak, at other times
risk is low)
Lyme disease causing spirochete Period of COMMUNICABILITY?
Place of EXIT
Route of pathogen out of reservoir toward the person to be infected.
Lyme disease causing bacteria exit from reservoir?
Place of EXIT for some other common infectious agents:
moisture droplets from mouth & nose, feces or direct physical contact
Mode of TRANSMISSION
How pathogen moves from reservoir to the person to unsuspecting recipient.
Lyme disease causing spirochete Mode of TRANSMISSION?
Mode of TRANSMISSION for some other common infectious agents:
air or surface carried moisture droplets from mouth & nose, or direct physical
contact, carried in dirt , food, water that is them ingested
Portal of ENTRY
How pathogen gets into recipient’s body.
Lyme disease causing spirochete Portal of ENTRY?
Portal of ENTRY for some other common infectious agents?
SUSCEPTIBILITY of host
Recipient of pathogen may not become sick if body is able to resist the infection by
specific or nonspecific body responses to pathogens e.g., inflammatory
response & immunity
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 4
updated 3/17/2010
Communicable Diseases
Lyme disease causing spirochete SUSCEPTIBLE hosts?
Which groups in the population are very susceptible hosts to infections?
INCUBATION PERIOD
Time between pathogen entry and symptom appearance
Lyme disease causing spirochete INCUBATION PERIOD?
varies greatly between pathogens
e.g., 1-3 day for cold
overlap with period of communicability varies
DISEASE 1
incubation
symptoms
communicability
DISEASE 2
incubation
symptoms
communicability
What is a special challenge to stopping disease #2?
What diseases fit this category?
SELECT A COMMUNICABLE DISEASE AND…
 WORK OUT EACH STEP IN THE DISEASE CYCLE
 IDENTIFY WHERE IN THE CYCLE THE SPREAD OF THE DISEASE CAN BE
ADDRESSED
HOW DOES THE BODY DEFEND AGAINST PATHOGENS?
PART A: NONSPECIFIC DEFENSES AGAINST BROAD CATEGORIES OF
PATHOGENS = NONSPECIFIC IMMUNITY
1) NOT BE SUSCEPTIBLE TO THE PATHOGEN
some pathogens are only able to infect certain species
e.g, some viruses that infect animals will not infect humans due to differences in
genetic material
2) MECHANICAL BARRIER
The intact skin and gut lining have tight junction between cells to prevent many
pathogens from passing easily to the interior of the body (remember, something
inside the gut is not yet inside the body)
Cilia “sweep” foreign pathogens from respiratory tract.
3) ENZYMES
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 5
updated 3/17/2010
Communicable Diseases
Enzymes in the stomach and tears destroy some pathogens trying to enter the
body through this route
AFTER A PATHOGEN HAS ENTERED YOUR BODY, WHAT CAN YOUR BODY DO?
4) INTERFERONS
proteins produced by cells infected by viruses, will reduce the chance of other cells
getting infected (a mechanism not well understood yet)
5) INFLAMMATION & PHAGOCYTOSIS
A tissue response to pathogenic injury (or mechanical) that prevents the spread of
the infectious agents, then removes the foreign material and killed cells
EXAMPLE OF NONSPECIFIC DEFENSE PROCESS:
pathogen enters body (e.g., through a cut)
macrophages & leukocytes are chemically attracted to the site (chemotaxis)
complement proteins in the blood promote destruction of bacteria
macrophages remove the foreign pathogen by phagocytosis
if infection is sufficiently large:
redness & warmth due to increased blood flow
swelling due to increased fluid movement into tissues as capillaries become more
permeable to allow leukocytes to move into tissue from blood stream
pus due to accumulation of dead leukocytes
fever due to chemical release from leukocytes
some believe that a mild to moderate fever is beneficial during a bacterial
infection, inhibiting bacterial growth
if infection is small, then the nonspecific immune response described above may
be sufficient to eliminate the pathogen
if infection is sufficiently large, then SPECIFIC IMMUNE RESPONSE IS
INITIATED, to allow antibodies specific to the invading pathogen to be
produced
HOW DOES THE BODY DEFEND AGAINST PATHOGENS?
PART B: DEFENSES AGAINST SPECIFIC PATHOGENS = SPECIFIC IMMUNITY
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 6
updated 3/17/2010
Communicable Diseases
BONE MARROW
erythrocytes
LEUKOCYTES (WHITE BLOOD CELLS)
platelets
stem
cell
IMMATURE LYMPHOCYTES (one class
of leukocytes)
Lymphocyte maturation in BONE
produces B-LYMPHOCYTE
(bone derived)
Lymphocyte maturation in THYMUS
produces T-LYMPHOCYTE
(thymus derived)
T-cell
Release to blood and accumulation
in lymph nodes & spleen (70-80% Tlymphocytes, most of the rest are
B-lymphocytes)
Two types of
lymphocytes for our
immune response:
B-cell = B-lymphocytes:
combat bacterial &
some viral infections
secrete antibodies into
blood & lymph
= humoral immunity =
antibody-mediated
immunity
T- cell = Tlymphocytes:
combat host cells
infected with viruses or
fungi, transplanted
human cells, and cancer
cells
do not secrete
antibodies, must come
physically close to the
cell to be attacked
= cell-mediated
immunity
B-cell
80% of lymphocytes are T-cells. These are critical for immunity, transplant rejection,
cancer and other situations. But we will focus on B-cells, because these are involved in
the development of immunity, our focus of discussion.
HOW B-LYMPHOCYTES & ANTIBODIES PROTECT YOU FROM INFECTIONS
BREAK IN SKIN ALLOWING
BACTERIA ENTRY
SKIN
ANTIGEN = molecule that
stimulates antibody production
usually a protein, e.g.,
protein on the surface of
a foreign bacteria
ANTIGEN ON SURFACE
B-lymp hocyte
with antibod ies on
all surfaces
= recep tors for
foreign (non-self)
antigens
bacteria with foreign (to
the host) p rotein on the
surface
Exposure of a B-Lymphocyte to
an antigen it is sensitive to
results in multiple cell
divisions to produce:
1) plasma cell: which produces
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 7
updated 3/17/2010
Communicable Diseases
antibodies which attach
to the antigen
2) memory cell: produce
antibodies for the
antigen faster next time
Next: a ntigen on ba cter ia binds to
a ntibodies on B-lymphocyte
B-lymphocyte
w ith a ntibodies on
a ll sur fa ces
= r eceptor s for
a ntigens
ba cter ia w ith for eign (to
the host) pr otein on the
sur fa ce
Next: B-lymphocyte divides many
time to produce PLASMA CELLS
& MEMORY CELLS, both of
which are specific to the specific
antigen (on the foreign pathogen)
which arrived
Memory
cell
Plasma
cell
PLASMA CELL: produce about
2 thousand antibodies
per second during 5-7
day life. Antibodies are
specific to bind with
antigen on foreign
material (protein in this
example).
MEMORY CELL: ready to
produce antibodies specific for
the foreign protein antigen (on
the foreign bacteria in this
example) if that foreign protein
shows it’s face (i.e., it’s antigen)
again.
Memory
cell
Plasma
cell
When antibodies bind to
foreign antigen on invading
pathogen, they do not kill the
pathogen, BUT THEY
IDENTIFY IT AS A FOREIGN
BODY, and this stimulates
COMPLEMENT proteins to kill
the foreigner.
Complement proteins also
stimulate MAST CELLS (a
connective tissue cell type) to
release HISTAMINE.
HISTAMINE causes
increased local blood flow,
attracts more phagocytes to
the area to the area, and
increased capillary
permeability, causing edema
(now you know why you
take antihistamines, see
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 8
updated 3/17/2010
Communicable Diseases
Next: Antibodies a tta ch to the specific a ntigen (on the
for eign pa thogen), to ma r k for for a tta ck by complement
(C) pr oteins. Complement stimula tes HISTAM INE r elea se.
M emor y cells w a it for next inva ision by sa me pa thogen.
M emor y
cell
Pla sma
cell
M emor y
cell
C
there are 100 million trillion
(1020) antibodies in each
person, representing specificity
for a few million different
antigens
C C
ba cter ia
C
HISTAMINE
RELEASE
discussion of allergies later)
MAST
CELL
C
C
C
Q: WHAT IS THE BIG DIFFERENCE BETWEEN THE FIRST & SUBSEQUENT
EXPOSURES TO A PATHOGEN?
DEVELOPMENT OF MEMORY CELLS WITH FIRST EXPOSURE, ALLOWING
FASTER RESPONSE TO NEXT EXPOSURE TO PATHOGEN IS TERMED
DEVELOPING IMMUNITY TO THAT PATHOGEN
IMMUNITY = protected from getting a disease because immune system can destroy
the pathogen before disorder & symptoms in the host
HOW DOES YOUR SPECIFIC IMMUNITY DEVELOP (IS IT ACTIVE OR PASSIVE
IMMUNITY)?
ACTIVE IMMUNITY
You ACTIVELY develop antibodies specific to a certain antigen through exposure
to the antigen
#1) NATURALLY ACQUIRED ACTIVE IMMUNITY
Exposure to the actual antigen, and you get the disease.
(process discussed above)
E.G., You get exposed to the mumps virus (from a sibling), you have the disease,
but in the process you develop antibodies to the virus. These antibodies (blueprint
for them actually) are stored in the memory cells specific for mumps. If the
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 9
updated 3/17/2010
Communicable Diseases
mumps virus invades your body again, your immune system is able to act quickly
and specifically to destroy the virus BEFORE it infects the body again.
YOU HAVE IMMUNITY TO THE MUMPS VIRUS, and will not get mumps again
#2) ARTIFICIALLY ACQUIRED ACTIVE IMMUNITY
= you develop immunity WITHOUT going through the disease
Exposure to the actual antigen accompanying weakened or dead pathogen =
VACCINATION.
E.G., Oral (Sabin) polio vaccine contains living polio viruses, which are attenuated
(too weak to cause disease). They have the protein antigens, so an immune
response is developed, and memory cells formed (YOU DEVELOP IMMUNITY
TO THE PATHOGEN) to combat successfully any subsequent exposure to the
polio virus.
BUT, the attenuated virus in the vaccine will not give you the actual polio disease
(in almost all cases).
other examples of vaccinations: diphtheria, pertussis (whopping cough), tetanus,
polio, rubella, measles, mumps, cholera, typhoid fever, hepatitis B
You should have a list of specific dates of your documented infection with these diseases,
or immunization schedule.
Check with your physician/nurse to see that you are up to date with the immunizations
you need
• tetanus immunizations (actually tetanus & diphtheria booster) must be updated
every 10 years
• was Hep B given to you? Probably not, the safe recombinant form is only a few
years old! Now recommended for all children. Strongly recommended for
health care workers, sexually active gay men, heterosexuals with multiple
partners (transmitted by contact with infected body fluids). (Both Hep A & B
cause liver damage)
• Hep A: a new vaccine. Needed by persons traveling in Mexico, Latin America,
Africa, eastern Europe, & other places where Hep A is common (due to fecal
contamination of food & water). Also persons with liver disorders and those
who have anal sex.
• new developments in the science of immunization mean that old immunizations
may be determined to be not as good as what is available currently, so get the
updated vaccine
PASSIVE IMMUNITY
You do not develop antibodies specific to a certain antigen, you get them ADDED to your
system to fight pathogens in your system
#1) ARTIFICIALLY ACQUIRED PASSIVE IMMUNITY
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 10
updated 3/17/2010
Communicable Diseases
The antibodies for a specific pathogen are injected into your system, they last a few days
to a few weeks. You have not developed your own immune response.
E.G., snake bite or tetanus antiserum (antitoxin)
#2) NATURALLY ACQUIRED PASSIVE IMMUNITY
The antibodies for a specific pathogen are passed from mother to baby. Baby has not
developed it’s own immune response.
E.G., Some of mother’s antibodies cross the placenta, last approximately 1 month
after birth. Some of mother’s antibodies are carried in the mother’s first milk (the
colostrum)
HOW DOES YOUR IMMUNE SYSTEM DISTINGUISH BETWEEN SELF
AND FOREIGN ANTIGENS?
Why do you not develop antibodies against yourself?
In the first month of life, when the immune system is developing, the immune system
learns to recognize “self” antigens and does not produce B & T cells for them
In some disorders, the immune system attacks self antigens as though they are foreign
= autoimmune disorders
e.g., rheumatoid arthritis, multiple sclerosis, insulin dependent (type I) diabetes
mellitus, myasthenia gravis, systemic lupus erythematosus
• the body produces antibodies or presents self tissue to T-lymphocytes, that try to
destroy the body’s own tissue
• cause unknown
FINAL COMMENTS ON A FEW SPECIFIC PATHOGENS:
: WHY DO WE KEEP GETTING COLDS & FLUS? IS OUR IMMUNE SYSTEM NOT
WORKING?
FLU (influenza): Kills 20,000 U.S. residents in a typical year. Caused by a virus that is
always changing shape (mutations), so no permanent vaccine is possible now. New flu
viruses are always developing, typically where humans live very close to animals,
especially pigs, Southern China is a major breeding ground for new flu viruses. But a
vaccine for the strain common that year can be developed and taken. Immunity useful
for that strain only. People who would really suffer (the elderly, people with immune
deficiency) from the flu should get the vaccine.
COLD: caused by a virus, so antibiotics don’t help. Cold viruses keep changing surface
antigens, so while we develop immunity to the cold virus that just made our week
miserable, a new virus comes along the next week, so we get the new cold.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 11
updated 3/17/2010
Communicable Diseases
EXERCISE & IMMUNITY
With emphasis on Upper Respiratory Tract Infections (URTI) (e.g., cold & flu)
The hypothesized relationship between URTI and exercise exertion is a “J” shaped
relationship.
inactive person has average rate of colds and flu
moderate activity levels reduce your rate of infection
extreme activity levels increase rates of infection above average.
WHAT EVIDENCE IS THERE FOR THIS HYPOTHESIS?
STRENUOUS EXERCISE LEVELS
acute strenuous exercise:
• raises blood epinephrine and cortisol levels
• these hormonal alterations depress immune function, lasting hours after
exercise
(decreases in ALL the following: leukocyte & lymphocyte levels in blood, t-cell
proliferation in response to pathogen, b-cell function, antibody levels,
complement levels)
following strenuous exertion you are more likely to experience a URTI
e.g., following marathon run
cumulative, repeated day-after-day strenuous physical exertion keeps the immune
system depressed
Hence: rise in infection rates with chronic high level training
WHAT LEVEL OF EFFORT DEPRESSES IMMUNE FUNCTION?
no set level, individual responses will vary
PLUS, physiological (training) effect COMBINES with mental stressors acting on
person (e.g., mental load of training, stress caused by competition)
& people will have different mental stressors, and ways of reacting to them.
MODERATE EXERCISE LEVELS, do they reduce risk of URTI?
FEW TO NO GOOD STUDIES THAT EXAMINE THIS QUESTION & PROVIDE SOLID
ANSWERS
SHOULD YOU EXERCISE WHEN YOU HAVE AN URTI?
MILD EXERCISE DURING SICKNESS:
does not appear to be bad
UNLESS: infection has spread beyond the URT to other body systems (e.g., fever,
extreme tiredness, muscle aches, swollen lymph glands)
THEN allow 2-4 weeks before intensive training to ensure virus has been eliminated
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 12
updated 3/17/2010
Communicable Diseases
if the virus is systemic, the risk of severe form of viral infection is HIGH e.g., viral
cardiomyopathy
STRENUOUS EXERCISE DURING SICKNESS:
VERY bad idea
severe form of viral infection is HIGH e.g., viral cardiomyopathy
e.g., military basic training: close quarters, lot of opportunity for viral infections to
spread, forced strenuous exercise, some people drop dead during training
1.6 million recruits, 19 sudden deaths, 2/3 (?) viral cardiomyopathy
PERSONAL WELLNESS ACTIONS FOR COMMUNICABLE DISEASES AT YOUR
WORKSITE
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 13
updated 3/17/2010
Allergies
TOPICS:
ALLERGIES
IMMEDIATE HYPERSENSITIVITY
TREATMENT FOR IMMEDIATE ALLERGIC REACTION
CAN YOU PREVENT ALLERGIES?
DELAYED HYPERSENSITIVITY
WELLNESS ACTIONS FOR ALLERGIES
ALLERGY = hypersensitivity of the immune response to an antigen
in this case the antigen is called an ALLERGEN
2 major forms of allergies:
1) IMMEDIATE HYPERSENSITIVITY
Occurs in seconds or minutes after exposure
Due to excessive B-lymphocyte response to antigen (allergen)
e.g., Hay fever (allergic rhinitis), commonly grass pollen allergin
Common allergens: dust mite poop, animal dander carrying animal saliva protein,
plant pollens
HAY FEVER: allergen is grass or tree pollen, ragweed, mold spores,
review of normal (non allergy) immune response to antigen
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 14
updated 3/17/2010
Allergies
NORMAL (NON ALL ERGY) IMMUNE RE SPONSE TO ANTIGE N
1) Foreign bacteria with
antigen
Plasma
cell
C
C
C
C
2) Prod uct ion of antibodi es to the
antigen
3) anti bod ies bind to foreign bod y at
antigen sit e, identi fy it as forei gn
CAPILL ARY
4) stimulation of compl ement proteins (C) to kil l
foreign cel l, & stimulate mast cell to prod uce
histamine
C
Mast
cell
C
C
HISTAMINE
C
5) Histamine release causes
increased capi llary permiabilit y, so
more phagocytes can move into
ti ssue, and allow l ocal swelli ng
6) Phagocyti c cell s engul f and di gest d ead
bacteria
Phagocyte
STEPS 1-3) FIRST EXPOSURE TO ALLERGIN
B-Lym phocyte
Plasm a
cell
1) Foreign particle with
allergin (antigen)
3) IgE antibodies bind to MAST CELL
2) Production of IgE antibodies to
the allergin
Mast
cell
HISTAMINE
STEP 4) ON SUBSEQUENT EXPOSURE TO ALLERGIN
Mast
cell
MECHANISM of
allergic response:
allergen stimulates
antibody production
by B-lymphocyte
antibodies to allergen
attach to mast cell
(because they are IgE,
not IgG) not to
antigen like in usual
response to antigen
Mast cell releases histam ine &
other chem icals to produce allergic
reaction
HISTAMINE
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
In a person who
Pg. 15
updated 3/17/2010
Allergies
SUBSEQUENT EXPOSURE TO ALLERGEN stimulates
mast cell to produce HISTAMINE (& other chemicals)
HISTAMINE causes itching, sneezing, runny nose (clear
thin fluid for allergy)
develops the allergy,
there is an excessive
production of these
antibodies, which then
allows the following
steps.
Histamine causes vasodilation & increased leakage of fluids
from blood vessels, if excessive blood pressure drops =
anaphylactic shock
therefore: some allergies CAN be fatal to some people (e.g,
allergies to food, stinging insects, drugs)
TREATMENT FOR IMMEDIATE ALLERGIC REACTION:
treat with antihistamine drug, to reduce histamine release
But antihistamines are often sedating
(newer, stronger, non sedating antihistamines are available by prescription)
FOOD ALLERGIES:
only 1% of adults (3% of children) have true allergies to food
food allergies have a significant genetic influence (i.e. inherited), breast feeding
reduces susceptibility
WHY DO WE DEVELOP ALLERGIES? {GENETICS + ENVIRONMENT}
 There is a genetic component to the development of many allergies
 A major hypothesis is that sensitization (exposure) to an allergen in early infancy
(even in utero) is a major contributor to the subsequent development of the allergy.
Therefore, avoiding exposure to allergens when an infant may help subsequent
allergies not develop.
2) DELAYED HYPERSENSITIVITY
Occurs within 1-3 days after exposure
Due to excessive T-lymphocyte response to antigen (allergen)
e.g., contact dermatitis (poison ivy, poison oak)
but some individuals can give allergic response following exposure to a wide variety of
common items (e.g., coins, plastics, cosmetics, leather, rubber, dyed clothing)
treatment: corticosteroids
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 16
updated 3/17/2010
Allergies
Mysteries of Allergies Studied
Sunday, May 19, 2002 12:02 p.m. EDT
By JUSTIN GLANVILLE Associated Press Writer
You wake up in the morning congested and sniffling. Your eyes itch. The roof of your
mouth burns. You sneeze.
It's allergy season, and pollen is in the air. Pollen is the archenemy of an estimated 20
million allergy sufferers in the United States
alone, according to the Columbia
University College of Physicians and Surgeons.
Why is your body so upset? How is it that your neighbor can mow the lawn without
batting an eye, while the very sight of cut grass sends you running for the medicine
cabinet?
"There's no simple answer," says Dr. Andrew Saxon
, chief of the UCLA School of
Medicine's Division of Clinical Immunology
and Allergy.
On one level, allergies remain a medical mystery. There's nothing
truly dangerous about pollen, dust, fur or most other common
allergens, so it's uncertain why some people's bodies treat them
as invaders. An allergen is anything that triggers an exaggerated,
and usually unnecessary, immune response.
But over the past several decades, Saxon and other researchers have made significant
progress toward explaining why allergies exist and why they have become so common.
Hard numbers are not available, but Saxon estimates that about 35 percent of the
population of the Western hemisphere suffer some form of allergy - up from about 25
percent in the 1970s. In the early 19th century, hay fever was so rare that it took one
early researcher, Jonathan Bostock, nine years to find enough subjects to publish a
study.
At that rate of increase, it seems clear that factors other than heredity - long identified
as a crucial determinant of whether one is allergic - are involved.
Pollution may be one important culprit. According to Saxon's research, breathing
irritants such as diesel exhaust sets the immune system on edge, increasing the
likelihood that it will overreact to potential allergens. "What diesel and other irritants
do is kick the immune system in the side, pushing it toward an attack," Saxon says.
His experiments, which began about 12 years ago, involved two groups of subjects.
One group was exposed only to an allergen. The other group was exposed to the
allergen and a whiff of diesel exhaust.
Those in the first group had only a "protective" immune response: Their bodies tended
not to identify the allergen as a potential threat. Those who also breathed exhaust, on
the other hand, were more likely to attack the allergen. Their bodies produced more
antibodies and they responded to a smaller amount of the allergen in the future.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 17
updated 3/17/2010
Allergies
Air quality has improved markedly in the United States since 1970. However, Saxon
has found that inhaling even small amounts of industrial pollution increases the
likelihood of an immune reaction.
Civilization may also be heightening people's sensitivity to so-called perennial allergens
- indoor particles such as dust, roaches, mold and dander (bits of animal skin). They
have become a widespread problem only in the last century or so.
"We think it may be related to the way homes are being built nowadays," says Dr.
Jacqueline Pongracic, acting manager of the division of allergies at Children's Memorial
Hospital in Chicago and a professor at Northwestern University.
"Homes are tightly sealed, with better systems of heating and cooling and less outside
ventilation. That increases the number of indoor allergens," she says.
"Also, modern society tends to have cats and dogs as indoor pets, whereas in older
times, animals were more outdoors, especially in rural areas."
Paradoxically, allergies may also be on the rise because health care for children is
improving.
How's that?
There are two main patterns of immune response - allergic and infectious. In children
who face many viral and bacterial infections, their immune systems may "learn" to
operate more in infectious mode than in allergic mode.
That can be beneficial because the infectious response is more of a destroyer than the
allergic response. Faced with an infection, the body identifies viruses and bacteria,
tries to kill them outright, and girds the body to eliminate invaders when they re-enter
the body. That's why people usually don't suffer the same infection, such as chicken
pox, twice.
The allergic response is more wishy-washy. The body identifies allergens as threats,
but doesn't have any means of protecting itself in the future. So the same allergen
usually plagues people for most of their lifetime.
All of which begs a question: Why does the allergic response
exist in the first place?
That remains a mystery. But it might have to do with worms.
"The hypothesis is that a long time ago, before civilization, people
evolved this hypersensitive response as a way of dealing with
parasites," Pongracic says. "But today we don't have much
exposure to parasites, so the response shifted to allergens."
People sometimes report that they outgrow their allergies in adulthood, but that is
usually an illusion, doctors say. Once the body is sensitized to an allergen, it's
programmed for life.
"The reason a lot of people perceive that they are outgrowing allergies is that they're
changing their lifestyles and habits," says Dr. Stanley Goldstein, an allergist in
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 18
updated 3/17/2010
Allergies
Rockville Centre, N.Y. and director of Allergy and Asthma Care of Long Island.
"Whereas they used to be out in the fields playing sports in high school, once they get
to college they're inside studying. Or they move out of their parents' house, where
they had once been allergic to the family pet."
But symptoms often taper off in old age, due to the general weakening of the immune
system - the same process that makes seniors especially vulnerable to disease. The
body isn't strong enough to react to allergens with the same gusto it did in childhood
and adulthood.
"So you get other diseases, but your allergies get better," Goldstein says wryly.
Still, according to Saxon, allergies are a small price to pay for improved pediatric
health and better home insulation. "Are we that bad off with allergies? No. I mean, in
the middle ages, people lived to 32."
--On the Net:
American Academy of Allergy, Asthma and Immunology: http://www.aaaai.org/
Asthma and Allergy Foundation of America: http://www.aafa.org/
Columbia University School of Medicine: http://www.medsch.ucla.edu/
Copyright © 2002 Associated Press. All rights reserved. This material may not be published, broadcast, rewritten,
or redistributed.
PERSONAL WELLNESS ACTIONS FOR ALLERGIES
& barriers to those actions
& hurdles to those barriers
Identify the role of the health professional
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 19
updated 3/17/2010
Allergies
IMMUNE SYSTEM WITH POTENTIAL TO EXCESSIVELY
REACT TO AN ANTIGEN
WHY?
GENETICS (INHERITED)
RANDOM CHANCE (BIOLOGICAL VARAIBILITY)
YES
NEED:
1ST EXPOSURE
TO PRIME MAST CELLS
2ND EXPOSURE
TO PRODUCE ALLERGIC
RESPONSE
FIRST EXPOSURE:
FOR SOME ALLERGIES IN
SOME PEOPLE THE FIRST
EXPOSURE MUST OCCUR
WHEN THE IMMUNE
SYSTEM IS DEVELOPING
(0-6 MONTHS)
E. G. , ?
POTENTIAL HERE TO
PREVENT FIRST EXPOSURE
AT CRITICAL TIME TO
PREVENT MAST CELL
PRIMING IN SOME PEOPLE
FOR SOME ALLERGIES, &
SOME PEOPLE THE FIRST
EXPOSURE CAN OCCUR AT
ANY AGE.
E. G. , ?
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 20
updated 3/17/2010
Asthma
Topics:
What is asthma?
Exercise induced asthma
What is asthma?
Asthma = bronchiolar constriction, which increases airway resistance to air flow, and
makes breathing (very) difficult.
Episodes can vary from mild (& lasting a few minutes) to severe, closing of the
airway, leading to unconsciousness & death.
typically in children (males mostly) under 10 yrs, but can continue into
adulthood
results is a few thousand deaths/yr. (4900 in 1992), but rate is increasing
CAUSED BY allergic response PLUS influence by psychological factors is common
Allergic response:
allergen causes allergic response (e.g., dust mites, pollen, food, mold, tobacco
smoke, mold) i.e., histamine release and LEUKOTRIENES, the latter causing
contraction of smooth muscles in the bronchioles
Leukotrienes: chemical released from mast cells not discussed previously
Psychological factors:
i.e., emotional states make the attack due to an allergic response worst
• some asthmatic children improve when removed from stressful family
situations
• some adult asthmatics experience more attacks when under stress
ASTHMA HAS 2 COMPONENTS:
1) Underlying inflammation of airway, not obvious, long term
2) Asthmatic episode, obvious, short lived
The ACUTE attack tends to be treated, but the chronic inflammation must also be
treated or the attacks will become more frequent and more severe.
Treat inflammation with steroids
Treat attack with bronchiole dilators
Why are rates of asthma increasing?
PERSONAL WELLNESS ACTIONS FOR ASTHMA
EXERCISE INDUCED ASTHMA (EIA)
10% of people (= 25 million Americans) are affected to some degree by EIA
EIA is a mild form of bronchial constriction and difficulty breathing
usually begins during exercise, or within 20 min following exercise, usually
abates within 30 min
EIA is more likely with high intensity exercise, & in cold dry air
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 21
updated 3/17/2010
Asthma
WHY DOES EIA OCCUR?
• rapid breathing of cold dry air may trigger release of chemicals causing
constriction of the bronchioles
• air pollutant or allergen may stimulate attack
PERSONAL WELLNESS ACTIONS FOR EIA:
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 22
updated 3/17/2010
Arthritis
Topics:
Arthritis
Rheumatoid arthritis
OsteoarthritisWellness actions
ARTHRITIS
strikes 1 in 3 Americans
nearly everyone > 40 years shows some
signs of osteoarthritis
costs the economy 10 billion per year
including > 1 billion spent on fraudulent
cures (seniors citizens are easy prey)
Rheumatoid arthritis (RA) = autoimmune disorder
antibodies attack synovial membrane tissues that produce fluids to lubricate the joints, later
damage to bone ends & articular cartilage causing:
inflammation, stiffness, pain, loss of movement, joint deformity
occurs in children, as well as adults (most common onset at ages 20-45), 3X more women
than men. 1% of all people
like most auto immune disorders, it may flair up, then go into remission, it may onset
quickly, or gradually.
CAUSES: genetic predisposition?, viral infection in joint?
TREATMENT: Pain relief (analgesics, massage, heat), immunosupression drugs, joint
replacement, bone fusion
Osteoarthritis (OA) = degeneration of the cartilage structures within joint
= gradual loss of smooth soft articular cartilage at the joint surface, frequent compensatory
overgrowth of bone.
Results in: painful range of motion, morning stiffness < 30 min, crepitance
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 23
updated 3/17/2010
Arthritis
85% of people 70-79 years old, especially in weight bearing joints, but also the hand
FACTORS WHICH MAY INFLUENCE DEVELOPMENT:
age (normal wear & tear?)
genetic predisposition (especially of hand OA)
direct injury to the joint tissue
chronic low level trauma to joint: occupational stress
e.g., increased & earlier hip, knee or hand osteoarthritis in: ♀ cleaners, ♀ in
clothing industry, ♂ masons, other construction workers, agriculture workers
(Rossignol et al., Primary osteoarthritis of hip, knee, and hand in relation to
occupational exposure. Occup Environ Med. 2005 Nov;62(11):772-7.)
being overweight: A 11 lb loss of weight in heavy people may decrease risk of
knee OA by 50% (Collins J., Exercise for the mind: are you joint smart? Semin Roentgenol.
2005 Jul;40(3):201-2)
ligament instability which alters the biomechanics of the joint may contribute to
premature OA
E.G, A SINGLE KNEE INJURY INCREASES RISK OF KNEE OA 5X
(Collins J., Exercise for the mind: are you joint smart? Semin Roentgenol. 2005
Jul;40(3):201-2)
TREATMENT: generally managed with analgesics, extreme cases require joint replacement
or fusion
Heat & massage may help symptoms
IS PHYSICAL ACTIVITY GOOD FOR OA?
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 24
updated 3/17/2010
Arthritis
When pain is controlled, stretching exercises are very
important for maintaining range of motion of the
joint, maintaining strength of the muscles
surrounding the joint is important because the person
will tend not to use them.
PLUS, person will obtain all the general
physiological & psychological benefits of aerobic
exercise
DOES PHYSICAL ACTIVITY PLAY A ROLE IN PROMOTING THE
DEVELOPMENT OF OA?
This is suggested by a number of anecdotal evidence & studies that suggested that activity
may lead to joint problems later in life.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 25
updated 3/17/2010
Arthritis
Studies examining this question must account for the influence of injury during activity and
subsequent joint misalignment.
BEST ADVICE: Reasonable activity, within limits of comfort, and without previous joint
problems, need not lead to joint injury (i.e., OA), and premature wearing out of joints, even
over many years.
WELLNESS ACTIONS FOR ARTHRITIS
 PREVENTION
 ACTIONS FOR THOSE WITH ARTHRITIS
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 26
updated 3/17/2010
Cardiovascular Disease
Topics:
Assessment of your cardiac risk
Normal function of the CV system
Cardiovascular (CV) disorders
Hardening of the arteries (arteriosclerosis)
High blood pressure (hypertension)
Heart attack (myocardial infarction)
Chest pain (angina pectoris)
Stroke (cerebrovascular accident)
Wellness actions related to CV disease
ASSESSMENT OF YOUR CARDIAC RISK
Do the test on the overhead to assess your risk level for cardiovascular disease, and to introduce
you to some of the issues we’ll be discussing.
question #6: assume total cholesterol is 200 mg, or estimate score based on amount of animal &
solid fats in diet
SCORE
1 Age
2 Heredity
3 Weight
4 Tobacco smoking
5 Exercise
6 Blood Cholesterol level or % fat in diet
7 Blood pressure
8 Sex, age, shape
TOTAL SCORE:
6 - 11 = very low risk
12 - 17 = low risk
18 - 25 = average risk
26 - 32 = high risk
33 - 42 = dangerous risk 43 - 60 = extremely dangerous risk
Note: more detailed assessment of CV risk may be obtained using the scoring scales provided by
the Framingham heart study. Available:
http://www.nhlbi.nih.gov/about/framingham/riskabs.htm
CARDIOVASCULAR (CV) DISORDERS
HARDENING OF THE ARTERIES (ARTERIOSCLEROSIS)
Several conditions (genetic & environmental risk factors) can lead to thickening & hardening
of the normally elastic arterial vessel walls as fat, mineral & cellular material
accumulates in the vessel wall.
The inner diameter of the vessel is reduced.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 27
updated 3/17/2010
Cardiovascular Disease
The hardened walls are less compliant to blood flow, and so contributes to hypertension
The narrowed lumen is more likely to be occluded by a clot, and so contributes to a heart
attack or stroke.
The process is a GRADUAL one that progresses over a life time
RISK FACTORS: Diet high in fat, especially saturated fat (animal fats and tropical oils (e.g.,
palm)), high blood pressure, smoking, lack of aerobic exercise, genetic influence
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 28
updated 3/17/2010
Cardiovascular Disease
New view of heart disease in women
Harvard Health Publications e-Newsletter. VOLUME 4 ISSUE 5 February 15, 2007
A revolution in thinking about coronary blood vessels could change the way women’s heart
problems are diagnosed and treated.
Discoveries from the WISE study suggest that many women have a form of heart disease called
coronary microvascular dysfunction that isn’t detected by standard diagnostic procedures and
thus goes unrecognized and untreated.
Causes of ischemic heart disease
Ischemic heart disease (IHD) is reduced blood flow to the heart. According to the classic model
of the disease, trouble begins when plaque builds up inside a coronary artery, which eventually
thickens and hardens, obstructing blood flow. The newer view of IHD suggests that the tiny
vessels feeding the heart can also become constricted and reduce blood flow.
Microvessel disease could also help explain why so few women have the classic crushing chest
pain that signals coronary artery disease. Instead, they feel diffuse discomfort, exhaustion, or
shortness of breath under stress or even during daily routines — symptoms that are nonspecific
and less dramatic than those that herald a blockage caused by a blood clot. As vessels lose their
resilience, blood flow is reduced, and the heart muscle, deprived of oxygen, gradually dies,
resulting in congestive heart failure.
HIGH BLOOD PRESSURE (HYPERTENSION)
Blood pressure = pressure exerted on the walls of the arterial vessels by the blood
peak pressure due left ventricle contraction = systolic pressure
low pressure between contractions = diastolic pressure
“typical” = 120/80 mm Hg
how many people here have had a BP taken in the last year by a professional (not in a
student lab)?
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 29
updated 3/17/2010
Cardiovascular Disease
Hardened, narrowed arteries (due to atherosclerosis) offer more resistance to blood flow,
which raises blood pressure (since the wall of the vessels don’t give as the blood flows
through)
this makes the heart need to work harder to push the blood
The high blood pressure then helps contribute to the development of further atherosclerosis
Hypertension
CAUSES OF HYPERTENSION: 90% of cases of hypertension are “essential” = no known
cause. 10% of cases related to other disorders (e.g., kidney, diabetes)
RISK FACTORS: Heredity (more likely if it is in family history), race (black more likely than
whites), high sodium in diet (only 10% of population is sodium sensitive, and so have BP
that responds to sodium they consume, but for others there is no reason to consume typical
high levels of sodium in diet), obesity, lack of aerobic exercise, alcohol
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 30
updated 3/17/2010
Cardiovascular Disease
Date: Feb. 11, 2004
Report Sets Dietary Intake Levels for Water, Salt, and Potassium
To Maintain Health and Reduce Chronic Disease Risk
WASHINGTON -- The vast majority of healthy people adequately meet their daily hydration needs by
letting thirst be their guide, says the newest report on nutrient recommendations from the Institute of
Medicine of the National Academies. The report set general recommendations for water intake based on
detailed national data, which showed that women who appear to be adequately hydrated consume an
average of approximately 2.7 liters (91 ounces) of total water -- from all beverages and foods -- each day,
and men average approximately 3.7 liters (125 ounces) daily. These values represent adequate intake
levels, the panel said; those who are very physically active or who live in hot climates may need to
consume more water. About 80 percent of people's total water comes from drinking water and beverages
-- including caffeinated beverages -- and the other 20 percent is derived from food.
"We don't offer any rule of thumb based on how many glasses of water people should drink each
day because our hydration needs can be met through a variety of sources in addition to drinking
water," said Lawrence Appel, chair of the panel that wrote the report and professor of medicine,
epidemiology, and international health, Johns Hopkins University, Baltimore. "While drinking water is a
frequent choice for hydration, people also get water from juice, milk, coffee, tea, soda, fruits, vegetables,
and other foods and beverages as well. Moreover, we concluded that on a daily basis, people get
adequate amounts of water from normal drinking behavior -- consumption of beverages at meals and in
other social situations -- and by letting their thirst guide them."
Regarding salt, healthy 19- to 50-year-old adults should consume 1.5 grams of sodium and 2.3 grams of
chloride each day -- or 3.8 grams of salt -- to replace the amount lost daily on average through
perspiration and to achieve a diet that provides sufficient amounts of other essential nutrients. Elevated
blood pressure, which may lead to stroke, coronary heart disease, and kidney disease, is
associated with sodium intake. On average, blood pressure rises progressively as salt intake
increases. A tolerable upper intake level (UL) -- a maximum amount that people should not exceed
-- is set at 5.8 grams of salt (2.3 grams of sodium) per day. Older individuals, African Americans,
and people with chronic diseases including hypertension, diabetes, and kidney disease are
especially sensitive to the blood pressure-raising effects of salt and should consume less than
the UL. More than 95 percent of American men and 90 percent of Canadian men ages 31 to 50, and
75 percent of American women and 50 percent of Canadian women in this age range regularly
consume salt in excess of the UL.
To lower blood pressure, blunt the effects of salt, and reduce the risk of kidney stones and bone loss,
adults should consume 4.7 grams of potassium per day. However, most American
women 31 to 50 years old consume no more than half of the recommended amount of
potassium, and men's intake is only moderately higher. Among foods with the highest
amounts of potassium per calorie are spinach, cantaloupes, almonds, brussels sprouts,
mushrooms, bananas, oranges, grapefruits, and potatoes. Canadians typically eat more
potassium than their American counterparts. African Americans in the United States generally get less
potassium than non-Hispanic whites, and because they have a higher prevalence of elevated blood
pressure, increased potassium intake may have particularly significant benefits for them.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 31
updated 3/17/2010
Cardiovascular Disease
The typical Western diet is high in salt and low in potassium -- the opposite of what evidence
shows is optimal for good health and reducing the risks of chronic disease, the report says.
"Research is needed to find ways to help people select better food choices to reduce their salt intake
and boost their potassium consumption," Appel said. In addition, because Americans and Canadians
get the majority of their salt -- 77 percent, according to one study -- from prepared and processed foods,
research should be done to help food processors develop alternative technologies that can reduce the
amount of salt added during processing without impairing taste, shelf-life, or product qualities at an
affordable cost.
[ This news release and report are available at http://national-academies.org ]
Sodium101.ca
http://www.sodium101.ca/
 Test of 6 foods
 Top Sodium Sources
HEART ATTACK (MYOCARDIAL INFARCTION)
Blood, & oxygen, supply to a portion of the myocardium is stopped due to a clot producing
an occlusion in the coronary artery
Often due to narrowing of the artery with arteriosclerosis
The myocardium downstream of the blockage is ISCHEMIC, myocardium dies without
oxygen
if a major coronary artery is blocked, then large amounts of myocardium dies, and the effect
is very serious, or fatal
if a minor coronary artery is blocked, then lesser amounts of myocardium dies, and the effect
is serious, but may not be fatal. The myocardium may have the opportunity to utilize it’s
COLLATERAL vessels to supply blood to the ischemic tissue
Major symptoms: severe chest pain, which may radiate to adjacent areas, dizziness, nausea,
pale, cold, rapid, shallow pulse
Immediately: obtain emergency care, start CPR if heart stops
RISK FACTORS: see risk factors for arteriosclerosis
CHEST PAIN (ANGINA PECTORIS)
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 32
updated 3/17/2010
Cardiovascular Disease
Chest pain occurs when the blood flow (& oxygen supply) to the myocardium is insufficient
(but not severe enough to cause a MI)
caused by restricted blood flow due to coronary atherosclerosis, combined with period of
stress, emotional upset or physical exertion
Treatment: drugs to dilate coronary arteries to increase blood flow
RISK FACTORS: see risk factors for arteriosclerosis
STROKE (CEREBROVASCULAR ACCIDENT)
Travelling clot lodges at atherosclerotic development, causes occlusion of an artery supplying
nervous tissue in the brain, elimination of oxygen supply causes cells to die.
Loss of function will depend on the region of the brain which was damaged, and the extent of
the damage.
Typically, stoke survivors may have loss of motor function (paralysis), speech, memory,
cognitive abilities.
Minor occlusions can lead to small strokes TRANSIENT ISCHEMIC ATTACKS (TIA)
seen as confusion, minor sensory or motor loss, temporary dizziness
Important for the individual, family member, or health care worker to recognize these
symptoms and have them seek medical help, because this is an early warning sign of the
disease process that will lead to more serious strokes.
RISK FACTORS: being black, high blood pressure, existing heart disease (reduces blood flow
to brain & increase probability of clots), & diabetes
THINK ABOUT:
 Sate the chances that you will suffer from CV disease
PERSONAL WELLNESS ACTIONS FOR CV DISEASE
[ANSWER AS A REVIEW OF PREVIOUS MATERIAL BEFORE READING ON]
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 33
updated 3/17/2010
Cardiovascular Disease
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 34
updated 3/17/2010
Cardiovascular Disease
RISK FACTORS WE CAN’T INFLUENCE: Heredity, increasing age, being male (at same age
prior to female menopause, male has higher risk)
genetics
environment
+
disease
Smoking, don’t do it. #1 lifestyle factor to contribute to CV disease
smoking damages lining of arteries, to contribute to atherosclerosis, it raises total cholesterol &
lowers HDL (HDL is the “good” cholesterol, which decreases risk of CV disease), reduces
oxygen content of the blood, increases heart rate, may constrict coronary arteries.
quitting is not easy due to addiction
Hypertension, avoid it, treat it.
avoiding hypertension:
treat hypertension: must know you have it, so have BP taken regularly, reduce salt intake,
maintain optimal body weight / regular exercise
Reduce saturated fat intake
where do saturated fats come from?
saturated fats have the effect of increasing the LDL (low density lipoprotein) cholesterol
component in the blood.
Reduce trans-fatty acid intake
what is an polyunsaturated fat?
to make fats more solid to make margarine, or to put them into foods, hydrogen atoms will be
added to remove double bonds, fewer double bonds are more solids at room temp
look at a food label & look for the word “hydrogenated”
Problem is that the process produces TRANS isoforms of fatty acids (cis- isoforms exist in
nature)
Trans isoforms of fatty acids increases the LDL (low density lipoprotein) cholesterol component
in the blood. LDL is the “bad” cholesterol, which increases risk of CV disease.
Use nonhydrogenated, or softest (least hydrogenated), margarine possible
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 35
updated 3/17/2010
Cardiovascular Disease
AEROBIC EXERCISE
Lack of aerobic exercise is an independent risk factor for CV disease, independent from it’s
effects on smoking, hypertension, diabetes etc.
Typical college students (and North Americans in general) are not active in regular aerobic
exercise.
THINK ABOUT: list 1 action you have done in the last month to improve your CV health.
THINK ABOUT: list 3 actions you can do in the next month to improve your CV health. This
must include one dietary action.
How easy do you think it will be to make these changes? Why do you think it will be easy or
difficult?
The following material to the end of this unit will be discussed if there is time in the
class. If it is not discussed, it will not be on the exam.
DIETARY FAT:
recommended: 20-35% of calories from fat
HOW CAN YOU TELL?
Looking at one food: see food label see: # calories, # fat calories
e.g., 120/260 * 100 = 46%
but this is one food only, the AVERAGE intake should be <=35% calories from fat.
How to figure this average?
and, how to do this for all foods your eat, how to do this for nonlabeled food eaten at restaurant?
USE A COMMON SENSE, NO CALCULATION APPROACH TO KEEPING YOUR FAT
INTAKE LOW (from the Berkeley Wellness Letter):
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 36
updated 3/17/2010
Cardiovascular Disease
HOW OFTEN DO YOU EAT THE FOLLOWING FOODS:
IF: NEVER, SELDOM, INFREQUENTLY & IN SMALL AMOUNTS
% calories from fat likely < 35%
hot dogs, sausages, luncheon meats, bacon, fried foods, hamburgers, fatty cuts of meats
(regular ground beef, corned beef, spare ribs, prime rib), cheese, donuts, cookies, cakes, pies,
pastries, oily or creamy salad dressings, potato chips, butter, margarine, whole milk,
premium ice cream, nuts, peanut butter
Common sense, no calculation approach #2 to keeping your fat intake low:
Learn to read food labels and be aware of content of foods you eat, keep a mental
running average
If food > 35% calories from fat - limit intake (pulls average up)
If food < 35% calories from fat - eat freely (pulls average down)
OTHER General Principles for changing eating habits to decrease % fat in diet:
Think of meats, poultry & fish as side dishes (not the center of the meal) to be consumed only
once per day
Increase consumption of grains, fruits & vegetables
Switch to nonfat or low fat dairy products
What are some of the road block to this? How to overcome them?
Does vegetarian food mean healthy?
OTHER INFLUENCES ON CV HEALTH BEING STUDIED
• 2-3 servings of fish per week, especially cold water fish (e.g., salmon, sardines (not oil packed),
lake trout, albacore tuna, whitefish)
lower fat & lower saturated fats than meat, omega-3 oils may be of some use in lowering risk of
CV disease, (but not as capsules)
• ANTIOXIDANTS: Vit E, C, beta carotene, selenium, polyphenols (& others)
IN: fruits, grains, vegetables, tea, coffee, wine (& other sources)
act as antioxidants, reducing free radicals in the body tissues
Free Radicals: cause LDL cholesterol to oxidize which promotes plaque buildup in vessel
walls (& free radicals may contribute to aging, cancer and other diseases)
• Alcohol: For men, up to 2 drinks per day is associated with reduced CV disease, by raising
HDL levels.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 37
updated 3/17/2010
Cardiovascular Disease
For women & men, Alcohol increases the risk of cancers of the mouth, pharynx (throat), larynx
(voice box), esophagus, liver, and breast, and probably of the colon and rectum. People who
drink alcohol should limit their intake to no more than 2 drinks per day for men and 1 drink per
day for women.
Regular consumption of even a few drinks per week is associated with an increased risk of breast
cancer in women, especially in women who do not get enough folate.
Women at high risk of breast cancer may want to consider not drinking any alcohol.
.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 38
updated 3/17/2010
Overweight & Obese
Why is obesity and overweigh such a prominent health issue today?
1. The incidence of people being obese or overweight is increasing rapidly.
2. There are significant health consequences of being obese or overweight.
What is “Overweight” & “Obesity”?
How to evaluate if a person is “Overweight” or “Obese”
Your body is composed of:
1. Fat-free mass
o Bone, water, muscle, connective tissue, organs,
teeth
2. Fat mass
o Essential Fat
 Fats in: nerves, brain, heart, glands etc.
o Non essential (storage) fat
 Fats is: fat cells  below skin and around organs.
How do you determine is someone is “Overweight” or “Obese”?
Body Mass Index (BMI)
BMI = body weight (kilograms) / height2 (meters)
BMI e.g., 5 ft 4 inch & 145 lbs
= 64 inches, 145 lbs
= 1.62 meters, 66 kg
= 66 / 1.62562
BMI = 25
The use of BMI to evaluate if a person is “Overweight”
or “Obese” is widely advocated by almost all major
health organizations, e.g., CDC
What is the BMI definition of “Overweight” & “Obese”?
BMI Cut points for Adults (> 18 years)
Source: http://www.cdc.gov/nccdphp/dnpa/bmi/bmi-adult.htm
Interpret BMI values for adults with one fixed number, regardless of age or sex, using the
following guidelines:
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 39
updated 3/17/2010
Overweight & Obese
Underweight
OK
Overweight
Obese
BMI less than 18.5
18.5 – 24.9
BMI of 25.0 to 29.9
BMI of 30.0 or more
Source: http://win.niddk.nih.gov/publications/understanding.htm#genetic
Positive aspects of using BMI to evaluate people?

Negative aspects of using BMI to evaluate people?

Height
6'3"
Weight
220 lbs
BMI
27.5
 Elderly people with low muscle mass and high body fat may be classified as
OK
How do you determine is someone is “Overweight” or “Obese”?
Body Composition Analysis
Body Composition Analysis to determine % body fat
Methods?
 Underwater weighing
 Skin folds
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 40
updated 3/17/2010
Overweight & Obese
 Bioelectric impedance
How is % body fat interpreted?
Percent Body Fat Standards*
Men
≤5%
6-14%
15%
16-24%
≥25%
At Riska
Below Average
Average
Above Average
At Riskb
Women
≤8%
9-22%
23%
24-31%
≥32%
At risk for diseases and disorders associated with malnutrition
a
At risk for diseases associated with obesity
b
*From Heyward, V.h. Advanced Fitness Assessment and Exercise Prescription. Champaign, IL: Human Kinetics.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 41
updated 3/17/2010
Overweight & Obese
Source
: Measurement for Evaluation in Physical Education and Exercise Science. Baumgartner, Jackson, Mahar, Rowe.
7th ed, McGraw Hill, 2003.
What is the incidence of American Adults that are overweight?
a) 15%
b) 35%
c) 65%
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 42
updated 3/17/2010
Overweight & Obese
Source: http://www.cdc.gov/nchs/products/pubs/pubd/hestats/obese/obse99.htm
Percent of adults ages 20–74* who were at a healthy weight, overweight, or obese†
*Data are age-adjusted to the 2000 U.S. standard population.
†Healthy weight, body mass index (BMI) = 18.5–24; overweight, BMI = 25–29; obese, BMI = >30.
Sources: National Health and Nutrition Examination Survey (National Center for Health Statistics);
Cancer Trends Progress Report — 2005 Update (National Cancer Institute 2005).
BMI > 30 2003
source: http://www.cdc.gov/nccdphp/dnpa/obesity/trend/maps/index.htm
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 43
updated 3/17/2010
Overweight & Obese
Overweight among Children:
Source: http://www.cdc.gov/nchs/products/pubs/pubd/hestats/overwght99.htm
Consequences for children:

Type 2 diabetes, previously considered an adult disease, has increased
dramatically in children and adolescents. Overweight and obesity are closely
linked to type 2 diabetes.

Overweight adolescents have a 70% chance of becoming overweight or obese
adults. This increases to 80% if one or more parent is overweight or obese.

The most immediate consequence of overweight as perceived by the children
themselves is social discrimination. This is associated with poor self-esteem and
depression.
Source: http://www.surgeongeneral.gov/topics/obesity/calltoaction/fact_adolescents.htm
Health risks of people being obese or overweight?
Overweight and obese individuals (BMI of 25 and above) are at increased risk for physical
ailments such as:
 Reduced life expectancy by 10-20 years.
o
o











An estimated 300,000 deaths per year may be attributable to obesity.
Even moderate weight excess (10 to 20 pounds for a person of average
height) increases the risk of death, particularly among adults aged 30 to 64
years
High blood pressure, hypertension
High blood cholesterol
Type 2 (non-insulin dependent) diabetes
Insulin resistance, glucose intolerance
Hyperinsulinemia
Coronary heart disease (even mildly to moderately overweight women have
80% increased risk of CHD)
Angina pectoris
Congestive heart failure
Stroke
Gallstones
Gout
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 44
updated 3/17/2010
Overweight & Obese







Osteoarthritis
Obstructive sleep apnea and respiratory problems
Some types of cancer (such as endometrial, breast, prostate, and colon)
Complications of pregnancy such as; gestational diabetes, gestational
hypertension and preeclampsia (A condition of hypertension occurring in
pregnancy, typically accompanied by edema and proteinuria.) as well as
complications in operative delivery (i.e., c-sections).
Poor female reproductive health (such as menstrual irregularities, infertility,
irregular ovulation)
Bladder control problems (such as stress incontinence)
Psychological disorders (such as depression, eating disorders, distorted body
image, and low self-esteem).
Overweight and obesity were found to be significantly associated with:
 Diabetes (discussed in another unit)
 High blood pressure (discussed in another unit)
 High cholesterol (discussed in another unit)
 Asthma (discussed in another unit)
 Arthritis (discussed in another unit) For every 2-pound increase in weight, the
risk of developing arthritis is increased by 9 to 13%.

Poor health status
Sources: http://www.cdc.gov/nccdphp/dnpa/obesity/consequences.htm
http://www.surgeongeneral.gov/topics/obesity/calltoaction/fact_consequences.htm
$ Cost of Overweight and obesity
$78.5 billion (1998) ($92.6 billion in 2002 dollars)
Source: http://www.cdc.gov/nccdphp/dnpa/obesity/economic_consequences.htm
The Duchess of Windsor once said, 'You can never be too rich or too thin.'
Possible negative consequences of excessive leanness.
 Reproductive disorders
 Circulatory disorders
 Immune system disorders
 Muscle wasting
 Fatigue
 Eating disorders
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 45
updated 3/17/2010
Overweight & Obese
Causes of overweight & obesity
Overweight and obesity are a result of energy
imbalance over a long period of time.
1.
2.
3.
4.
Causes of Energy in > Energy out, resulting in overweight & obesity
Genetic factors
Physiological factors
Lifestyle factors (=Behavior)
Psychosocial factors
Causes of overweight & obesity
1. Genetic factors
Heredity plays a role in determining how susceptible people are to overweight and
obesity (5% - 40% contribution???). “.Heredity plays a large role in determining how
susceptible people are to becoming overweight or obese”
http://www.cdc.gov/nccdphp/dnpa/obesity/faq.htm#factors
Genes also influence how the body burns calories for energy or stores fat.
e.g., the weight of an adoptee is more like that of the biological parent than the
adoptive parents
"Despite obesity having strong genetic determinants, the genetic composition of the
population does not change rapidly. Therefore, the large increase in . . . [obesity] must
reflect major changes in non-genetic factors."
http://www.cdc.gov/nccdphp/dnpa/obesity/contributing_factors.htm
Causes of overweight & obesity
2. Physiological factors
o Metabolism
o Hormones
o Fat Cells
METABOLISM:
Resting Metabolic Rate (RMR) = 55-75% of daily energy burned
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 46
updated 3/17/2010
Overweight & Obese
RMR is higher for:
 Some people due to genetics (you can’t control this)
 Men (higher due to increased muscle mass) (you can’t control this)
 Heavier people (more body tissue) (heavy people want to reduce this)
 People who exercise ?????
HORMONES:
 Hormones play a role in fat accumulation & distribution; this is
obvious at puberty & menopause when sex hormone levels change.
 LEPTIN – a hormone released by fat cells is thought to be a feedback
system, communicating from the fat cells to the brain, telling how
large the fat stores are, allowing brain to regulate appetite and
metabolic rate.
FAT CELLS:
 There is variation n the # of fat cells people have. It has NOT been
demonstrated that having more fat cells is a factor that drives people
to eat more.
Causes of overweight & obesity
3. Lifestyle factors (=Behavior)
A. Eating
B. Physical activity
C. Environment
A.) EATING influences:
In America, a changing environment has broadened food options and eating habits.
Grocery stores stock their shelves with a greater selection of products. Pre-packaged foods, fast
food restaurants, and soft drinks are also more accessible. While such foods are fast and
convenient, they also tend to be high in fat, sugar, and calories. Choosing many foods from
these areas may contribute to an excessive calorie intake.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 47
updated 3/17/2010
Overweight & Obese
Portion size has also increased. People may be eating more during a meal or snack because of
larger portion sizes.
Examples of common food options and eating habits
Bacon Double Cheeseburger
Vanilla Shake (Large)
French Fries (King)
Dutch Apple Pie
Calories
570
800
600
300
TOTAL
2270
If you go to your neighborhood McDonald's restaurant and order the Big Xtra meal, you
will get a sandwich, a large order of french fries and a large Coke. This meal contains:
710 calories in the sandwich
540 calories in the french fries
 310 calories in the drink
 630 calories in a M&M McFlurry
for dessert
TOTAL = 2190 calories


The calories required in one day are:
1,600 calories is about right for many sedentary women and some older adults.
2,200 calories is about right for most children, teenage girls, active women, and many sedentary
men. Women who are pregnant or breastfeeding may need somewhat more.
2,800 calories is about right for teenage boys, many active men, and some very active women.
Source: http://www.pueblo.gsa.gov/cic_text/food/food-pyramid/main.htm
B. PHYSICAL ACTIVITY influences:
Physical activity is any bodily movement produced by skeletal muscles that results in an
expenditure of energy with a range of activities such as
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 48
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Overweight & Obese



Occupational work, Carpentry, construction work, waiting tables, farming
Household chores, Washing floors or windows, gardening or yard work
Leisure time activities, Walking, skating, biking, swimming, playing Frisbee, dancing
Structured sports or exercise Softball, tennis, football, aerobics
Modernization, the growth of industry and technology, was introduced over 50 years ago in the
Western world. and has led to a decrease in overall physical activity
In 2000 more than 26% of adults reported no leisure time physical activity.
A significant world-wide decrease is observed in Physical Activity practices among young
people, especially in poor urban areas. A low level of physical activity is particularly common
in teenage girls. It is estimated that in a great number of countries, less than one third of young
people are sufficiently active to benefit their present and future health and well-being. Very
importantly, physical education and other school-based physical activities are decreasing.
http://www.obesity.org/subs/fastfacts/obesity_global_epidemic.shtml
http://www.cdc.gov/nccdphp/dnpa/obesity/contributing_factors.htm
http://www.who.int/moveforhealth/about/2004/en/
C. ENVIRONMENT influences:
Home, work, school, or community can provide barriers to, or opportunities for, an active
lifestyle.
Home
Schools
Work
Community
Ways to improve environmental factors contributing to weight gain
 Reduce time spent watching television and in other sedentary
behaviors
 Build physical activity into regular routines
 Ensure that the school breakfast and lunch programs meet
nutrition standards
 Provide food options that are low in fat, calories, and
added sugars
 Provide all children, from prekindergarten through grade
12, with quality daily physical education
 Create more opportunities for physical activity at work
sites
 Promote healthier choices including at least 5 servings of
fruits and vegetables a day, and reasonable portion sizes
 Encourage the food industry to provide reasonable food
and beverage portion sizes
 Encourage food outlets to increase the availability of lowcalorie, nutritious food items
 Create opportunities for physical activity in communities
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 49
updated 3/17/2010
Overweight & Obese
Causes of overweight & obesity
4. Psychosocial factors
 Food may be used in response to, or to regulate emotions, not being
controlled by calorie needs.
 Obesity is more prevalent at lower income levels.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 50
updated 3/17/2010
Overweight & Obese
SUMMARY: Causes of Energy in > Energy out, resulting in overweight & obesity
 Genetic factors
 Physiological factors
 Lifestyle factors(=Behavior)
Eating
Physical activity
Environment

Psychosocial factors
Behavioral and environmental factors are the main contributors to
overweight and obesity and provide the greatest opportunities for
prevention and treatment.
http://www.cdc.gov/nccdphp/dnpa/obesity/faq.htm#why
http://www.cdc.gov/nccdphp/dnpa/obesity/contributing_factors.htm
Genetics and the environment may increase the risk of personal weight gain, and may
make weight control more of a challenge for some people. However, the choices a
person makes in eating and physical activity also contributes to overweight and
obesity.
http://www.cdc.gov/nccdphp/dnpa/obesity/contributing_factors.htm#Environment
Healthy Weight Management



Diet & Eating Habits
Physical Activity
Thinking, emotions, coping strategies
Healthy Weight Management
 Diet & Eating Habits
Diet = daily food choices
Dieting = some form of food restriction
Basis for a healthy diet that allows for weight management:
1. Use the food pyramid as a basis for planning (to be revised Spring 2005)
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 51
updated 3/17/2010
Overweight & Obese
2. To keep energy in balance, pay attention to:
Total calories taken in balances energy expenditure
Best way to lose weight = moderate calorie restriction + increase in physical
activity
e.g., A difference of one 12-oz. soda (150 calories) or 30 minutes of brisk
walking most days can add or subtract approximately 10 pounds to your
weight each year.
To watch or reduce your calorie intake, pay attention to:
a) Portion size
A healthy portion size is usually smaller than the portion size served
b) Energy density
Consumption of a certain weight &/or volume of food makes you feel full and
satisfied.
So eat:
Food with a low # calories per volume
e.g.) increase consumption of: fruits & vegetables
reduce consumption of: Meat, ice cream, cookies, chips
c) Fat & sugar (carbohydrates) intake
Limit fat intake, to < 35% of total calories
Consume unsaturated fats (plant and fish fats)
DO NOT TRUST BOX LABELS SAYING “LOW FAT” OR “NON-FAT”.
While these products will be required by law to be low fat or non-fat, they
are often high in calories due to added sugars.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 52
updated 3/17/2010
Overweight & Obese
Simple carbohydrates (single or short chain sugar molecules) are broken down quickly by
the body to be used as energy. Simple carbohydrates are found naturally in foods such as
fruits, milk, and milk products. They are also found in processed and refined sugars such
as candy, table sugar, syrups, and soft drinks. Refined sugars are often called "empty
calories" because they have little to no nutritional value.
Complex carbohydrates are made up of sugar molecules that are strung together in long,
complex chains.
Complex carbohydrate foods provide vitamins, minerals, and fiber that are important to the
health of an individual.
Of the recommended 45% - 65% of your calories coming from carbohydrates:
The majority of carbohydrates should come from complex carbohydrates (starches)
and naturally occurring simple carbohydrates, rather than processed or refined
sugars, which do not have the vitamins, minerals, and fiber found in complex
and natural carbohydrates.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 53
updated 3/17/2010
Overweight & Obese
d) Protein Intake
Limit protein intake to recommended 10% - 35% of calories
 Meat foods high in protein are often high in fat
 Additional protein is not necessary
e) Eating habits
 Small, frequent meals on a regular schedule.
 Skipping meals, promotes snacking
Healthy Weight Management
 Physical Activity
Increase activity in daily activities (take stairs, park further away & walk more,
house work, gardening, etc.)
Add in a formal exercise program (aerobic, then resistance training).
Healthy Weight Management
 Thinking, emotions, coping strategies - to help with weight management
Developing positive, realistic goals and beliefs about yourself, and developing
positive problem solving skills
Have adequate and appropriate strategies to cope with life’s stresses and
challenges, so you do not rely on eating (or other unhealthy habits) to cope.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 54
updated 3/17/2010
Overweight & Obese
Hot Topic: High Fructose Corn Syrup
Sunday, December 4, 2005
SUSAN JOUFLAS / THE SEATTLE TIMES
High-fructose corn syrup fueling obesity epidemic,
doctors say
By Carolyn Poirot
Knight Ridder Newspapers
FORT WORTH, Texas — High-fructose corn syrup isn't completely
responsible for the nation's 6 million overweight children — but Dr.
George Bray says it's a big part of the problem.
Nurture trumps nature in the current childhood-obesity epidemic, says Bray. It's the
environment we're creating for our kids that's the problem, and that
environment includes increasing numbers of products high in highfructose corn syrup, or HFCS.
Bray, who served as founding president of the North American Association for the
Study of Obesity and organized the first international congress on obesity in 1973,
points out that between 1970 (when HFCS was introduced) and 2000
(when average yearly consumption of the ultra-sweet liquid sugar hit
73.5 pounds per person in this country), the prevalence of obesity
more than doubled, from 15 percent to almost one-third of the adult
population.
And worse, much worse, obesity among children 12 to 19 — who consume a
disproportionate amount of the soft drinks, fruit juice, sports drinks and packaged
cookies and other baked goods that are sweetened with HFCS — increased from 4.2
percent in 1970 to 15.3 percent in 2000.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 55
updated 3/17/2010
Overweight & Obese
American Journal of Clinical Nutrition, Vol. 79, No. 4, 537-543, April 2004
© 2004 American Society for Clinical Nutrition
Consumption of high-fructose corn syrup in beverages may play a
role in the epidemic of obesity1,2
George A Bray, Samara Joy Nielsen and Barry M Popkin
1
From the Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA
(GAB), and the Department of Nutrition, University of North Carolina, Chapel Hill (SJN and BMP).
Obesity is a major epidemic, but its causes are still unclear. In this article, we
investigate the relation between the intake of high-fructose corn
syrup (HFCS) and the development of obesity. We analyzed food
consumption patterns by using US Department of Agriculture food consumption tables
from 1967 to 2000. The consumption of HFCS increased > 1000% between 1970 and
1990, far exceeding the changes in intake of any other food or food group. HFCS now
represents > 40% of caloric sweeteners added to foods and beverages and is the sole
caloric sweetener in soft drinks in the United States. Our most conservative estimate of
the consumption of HFCS indicates a daily average of 132 kcal for all Americans aged
2 y, and the top 20% of consumers of caloric sweeteners ingest 316 kcal from
HFCS/d. The increased use of HFCS in the United States mirrors the
rapid increase in obesity. The digestion, absorption, and metabolism
of fructose differ from those of glucose. Hepatic metabolism of
fructose favors de novo lipogenesis. In addition, unlike glucose,
fructose does not stimulate insulin secretion or enhance leptin
production. Because insulin and leptin act as key afferent signals in
the regulation of food intake and body weight, this suggests that
dietary fructose may contribute to increased energy intake and
weight gain. Furthermore, calorically sweetened beverages may enhance caloric
overconsumption. Thus, the increase in consumption of HFCS has a temporal relation
to the epidemic of obesity, and the overconsumption of HFCS in calorically sweetened
beverages may play a role in the epidemic of obesity.
FIGURE 1. Availability of total fructose (•), high-fructose corn syrup (HFCS; ), and free
fructose ( ) in relation to obesity prevalence (x) in the United States.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 56
updated 3/17/2010
Overweight & Obese
Obes Res. 2004 Nov;12 Suppl 2:124S-9S.
Carbohydrates and increases in obesity: does the
type of carbohydrate make a difference?
Wylie-Rosett J, Segal-Isaacson CJ, Segal-Isaacson A.
Department of Epidemiology and Population Health, Albert Einstein College of
Medicine, Bronx, NY 10461, USA. [email protected]
With the prevalence of obesity increasing in the U.S. and elsewhere, the place
of carbohydrates in the diet has recently been under closer examination. This
has led to the development of methods for analyzing the effects of dietary
carbohydrate. Primary among these methods is the glycemic index, a measure
of a food's effect on blood glucose levels, which was initially designed as a
method for determining suitable carbohydrates for people with diabetes.
However, the glycemic index does not address other metabolic issues related
to excess sugar consumption. Prominent among these issues is the use of low
glycemic index sweeteners, particularly fructose, which is increasingly present
in processed food. Fructose is associated with increased adiposity, which
may result from its effects on hormones associated with satiety. Other
methods of determining "good" carbohydrates have also been developed. The
common theme among them is increased nonstarchy vegetables and higherfiber legumes.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 57
updated 3/17/2010
Overweight & Obese
Wellness Facts, September 2004
There is much debate these days about just how
bad sugar is, but one thing is not disputed:
Americans eat too much of it, 50% more than a
half century ago. Say the word sugar and most people think of the refined
white granules (sucrose) made from cane or beets. We actually eat much less of this
sugar than we used to. What we’re mostly overeating is fructose, the main sugar found
naturally in fruit and honey. It’s not that we’re eating lots of fruit, but rather millions of
tons of high-fructose corn syrup (HFCS), which is added to so many foods. This
sweetener now supplies nearly 10% of all calories consumed by Americans. The figure
is closer to 20% for some people, including many children. Those excess daily calories
are bad enough. But, in addition, preliminary research suggests that HFCS may be
worse for you than regular sugar.
HFCS is a liquid sweetener made from corn starch. Corn contains little fructose, but
manufacturers use a special process to boost the fructose content and thus make it
sweeter. About 70% of HFCS ends up in soft drinks; it’s also used in everything from
baked goods and candies to breakfast cereals and pasta sauces. HFCS is so widely
used because it is cheap (corn as a crop is subsidized by the government, and we grow
more of it than we can use), sweeter than sucrose, and easy to handle and blend with
other ingredients. Thirty years ago we consumed almost no HFCS, but now it is
pushing refined sugar aside as the No.1 additive in our food supply. The average
American consumes more than 62 pounds of it each year.
What’s wrong with HFCS, besides the calories
The body uses fructose differently than it does
other sugars, in part because fructose doesn’t
stimulate insulin secretion. This used to be considered a good
thing: for instance, small amounts of fructose can help improve blood sugar control in
people with Type 2 diabetes. But animal studies have found that large amounts of
fructose actually impair blood sugar control, and may promote high blood pressure.
Studies on humans suggest that high levels—as in large amounts of HFCS-sweetened
soft drinks—can boost triglycerides (fats in the blood) and possibly cholesterol. There’s
even some evidence that, in large quantities, fructose may not be as filling as sucrose
and thus may encourage overeating. In fact, some researchers point to the increased
consumption of HFCS as a prime culprit in the rising obesity rate. And if that isn’t
enough, high-fructose diets may have a negative effect on the body’s ability to use
calcium, chromium, and other minerals.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 58
updated 3/17/2010
Overweight & Obese
IFIC Foundation
http://if ic.org July / August 2004
What Do We Know About Fructose And Obesity?
Start of article not included here, see web site to obtain full article
Because nearly identical amounts of glucose and fructose are found
in sucrose and the HFCS used in beverages, similar results would be
expected with the types of HFCS commonly used in soft drinks. (i.e.
similar biological effects of fructose intake can be expected if
sucrose or HFCS were used to sweeten food products because
fructose intake will be similar). This remains to be tested.
Sucrose (table sugar) = 50% glucose and 50% fructose
Disaccharide = 2 bonded monosaccharides
High fructose corn syrup 42 (baking) = 42 % fructose, 58 % glucose;
HFCS 55 (beverage) = 55 % fructose, 45 % glucose
2 mixed monosaccharides (not chemically bonded)
HFCS is produce by a chemical reaction that converts some of the glucose in corn
syrup to fructose
Obesity is a complex issue with many contributing factors ranging from
genetics, social issues, food consumption, and physical activity. As
indicated previously in this article, the HFCS in the food supply does not
appear to be a major contributor to the increased energy intake of the U.S.
population. Many societal as well as dietary changes have occurred since
the 1970s that could be contributing to energy imbalance and development
of obesity. Changes affecting caloric intake also include: more meals
eaten away from home, larger portion sizes, and the relatively inexpensive
and abundant food supply. There are also other changes working to
reduce energy expenditure: increased reliance on the automobile, cuts in
physical education, more “screen time” (television, computers, and video
games), more hours working at sedentary jobs, more long distance
commuting, and more labor saving devices. Finally, other changes may be
contributing to both increased calorie intake and reduced energy
expenditure: more sleep deprivation, more night work, certain prescription
medicines, and emotional stress. With so many changes, it may be
overly simplistic to advocate a major causal role for any one food,
food ingredient, or nutrient in the obesity epidemic.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 59
updated 3/17/2010
Overweight & Obese
Oregon State University: Food Resource
http://food.oregonstate.edu/sugar/hfcs.html
“The truth is table sugar and HFCS are both about 50% fructose and 50%
dextrose (D-glucose). An analysis of annual HFCS 55 & 42 production
would reveal an average content of 49% fructose-nearly identical to the
fructose content of sucrose.”
i.e., A switch from sucrose to HFCS as a major sweetener does not
change fructose intake levels
Fructose is sweeter than sucrose (if not heated), but statistics from
the USA suggest that people do not cut back sugar use when they
use fructose.
http://www.medbio.info/Horn/Time%201-2/carbohydrate_metabolism.htm
1) Fructose,
insulin resistance, and metabolic dyslipidemia
Heather Basciano
, Lisa Federico
and Khosrow Adeli
Nutrition & Metabolism 2005, 2:5
doi:10.1186/1743-7075-2-5
The electronic version of this article is the complete one and can be found online at:
http://www.nutritionandmetabolism.com/content/2/1/5
Obesity and type 2 diabetes are occurring at epidemic rates in the United States and many parts of the
world. The "obesity epidemic" appears to have emerged largely from changes in our diet and reduced
physical activity. An important but not well-appreciated dietary change has been the substantial increase
in the amount of dietary fructose consumption from high intake of sucrose and high fructose corn
syrup, a common sweetener used in the food industry. A high flux of fructose to the liver, the main organ
capable of metabolizing this simple carbohydrate, perturbs glucose metabolism and glucose uptake
pathways, and leads to a significantly enhanced rate of de novo lipogenesis and triglyceride (TG)
synthesis, driven by the high flux of glycerol and acyl portions of TG molecules from fructose catabolism.
These metabolic disturbances appear to underlie the induction of insulin resistance commonly observed
with high fructose feeding in both humans and animal models. Fructose-induced insulin resistant states
are commonly characterized by a profound metabolic dyslipidemia, which appears to result from hepatic
and intestinal overproduction of atherogenic lipoprotein particles. {Chalmers notes: Liver fructose
metabolism is the same whether fructose comes from sucrose or HFCS} Thus, emerging
evidence from recent epidemiological and biochemical studies clearly suggests that the high dietary
intake of fructose has rapidly become an important causative factor in the development of the metabolic
syndrome. There is an urgent need for increased public awareness of the risks associated with high
fructose consumption and greater efforts should be made to curb the supplementation of packaged
foods with high fructose additives. The present review will discuss the trends in fructose consumption,
the metabolic consequences of increased fructose intake, and the molecular mechanisms leading to
fructose-induced lipogenesis, insulin resistance and metabolic dyslipidemia.
2) Carbohydrate metabolism lesson by Biochemistry professor.
http://www.medbio.info/Horn/Time%201-2/carbohydrate_metabolism.htm
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 60
updated 3/17/2010
Overweight & Obese
3) Elliott, S. S., Keim, N. L., Stern, J. S., Teff, K., & Havel, P. J. (2002). Fructose,
weight gain, and the insulin resistance syndrome. American Journal of Clinical
Nutrition, 76, 911-922.
Sources 1, 2, 3 above describe:
No difference in metabolism of fructose from sucrose versus from HFCS, both
fructose sources grouped and discussed together when fructose metabolism
explained. (diagram)
Sources 1, 2, 3 above agree that an elevated fructose intake is very bad due to:
 increased blood lipid levels
 fructose does not stimulate insulin release, which means lack of insulin
mediated leptin release, producing less appetite supression
 increased body weight
 insulin resistance
 and other effects
http://www.cdc.gov/nccdphp/dnpa/nutrition/pdf/r2p_sweetend_beverages.pdf
CDC 2006: No mention that HFCS offers an increased risk over other sugars present
in beverages. Recommended that people “Replace Sugar-Sweetened Beverages with
Water or Low-Calorie Beverages”
Added sweeteners. Are high-fructose corn syrup and other sweeteners fueling
the American obesity epidemic?: Harvard Health Letter. Oct. 2006;31(12):1-3.
No mention that HFCS offers an increased risk over other sugars present in a
beverage. Recommended that people “Reduce consumption of Sugar-Sweetened
Beverages & foods”, including those sweetened with fruit-juice concentrates. Drink
water”.
American Dietetic Association 2009
Kristine S. Clark, High Fructose Corn Syrup, (2008) Retrieved from:
http://www.eatright.org/cps/rde/xchg/ada/hs.xsl/nutrition_19399_ENU_HTML.htm
“High fructose corn syrup may be used as a sweetener in processed foods and beverages and
is nutritionally equivalent to sucrose. Both sweeteners contain the same number of calories (4
per gram) and consist of about equal parts of fructose and glucose. Once absorbed into the
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
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Overweight & Obese
blood stream, the two sweeteners are indistinguishable. No persuasive evidence supports the
claim that high fructose corn syrup is a unique contributor to obesity, however, like all nutritive
sweeteners, it does contribute calories. This is where moderation and portion size become
important.”
What do George Bray and Barry Popkin NOW say about the
role of HFCS in the development of the obesity epidemic?
Source: Warner, M., A sweetener with a bad rap, IFIC Foundation, http://ific.org Jan /
Feb 2007
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 62
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Overweight & Obese
IS: High-fructose corn syrup fueling obesity
epidemic?
Chalmers’ conclusion
 Fructose is metabolized very differently from glucose (remember fructose is not
HFCS)
 Elevated levels of fructose intake in the current diet is a contributing factor to
obesity (and associated metabolic disorders)
Would we be having the obesity epidemic IF HFCS were never invented?

The switch from sucrose to HFCS should not be blamed for the elevated fructose
intakes (IFIC article).
o If HFCS was never invented, we would be having the same obesity
epidemic, if we had the same high eating (and low physical activity) patterns,
and food was instead sweetened with sucrose, because fructose intake and
metabolic effects of fructose would be the same with sucrose sweetening
(IFIC article “this remains to be tested”)
“Fuel” for obesity epidemic:
a) Increased eating (more total calories = more fats + more sugars)
b) Decreased physical activity
c) Environmental changes that lead to (a) & (b).
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 63
updated 3/17/2010
Diabetes
Diabetes note will be distributed if Dr. Chalmers covers this topic. Otherwise, Dr. Li
will cover it in the second half of the class.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 64
updated 3/17/2010
HLED 345: RESEARCH PAPER ON A DISEASE OR HEALTH ISSUE: GRADING SHEET
Introduction
Yes & good ___(0 points)
Weak
Facts & detail do not
explain issues, or some
significant errors.
Presentation with very
significant errors
2
Comments
Yes but weak ___(-2 points)
Missing
NAMES:
Exceptional
Good
Adequate
Obvious extra
Correct facts at
Facts & detail explain issues,
& outstanding
sufficient detail to
but more detail, easily
effort in
explain issues, and
possible, or some explanation
research &
presentation without
confusing. Presentation with
reporting
any significant errors
some significant errors
5
4
3
5 4 3 2 1
FACTUAL CONTENT
(cover in the order listed)
TOPIC
Needs Help!
The term papers are to be turned into the PEHR
office (CV 102) by 5 pm on the date they are due.
1
0
No ___(-4 points)
Individual Vulnerability. Who is
vulnerable-e.g., age, gender, occupation,
ethnic origin, SES
Suggested and/or established
cause(s)
Symptoms & severity of the
disease/illness
Methods / procedures used to
diagnose the disease / illness
Scientifically proven treatments, to
eliminate, reduce severity or control disease
Prognosis
Suggestions for preventing
acquisition and development of the
disease / illness
PREPARATION OF PAPER
Paper and paragraph organization of
material, use of headings (listed
above) to organize material is
REQUIRED. Spelling,
punctuation, & sentence structure
Minimum nine citations, at least 4
peer reviewed journal articles, all
internet sources high quality
Citation list and in text citations
follow style defined in assignment
description (i.e., superscript #s in text,
numbered reference list).
Neatness of paper: arrangement of margins, spacing, use of headings and quality of font (i.e., blurred, broken or
faint printing is not acceptable)._____
1.5 pages _____
Grading sheet attached _______
(Maximum = 48 points)
General Comments (if any) on Reverse.
HLED 345 Lecture Notes  2010, Gordon Chalmers, Ph.D.
Pg. 65
updated 3/17/2010